Phenolic Acidin Teaand Coffeeand Their Health Benefits

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Phenolic acids in tea and coffee and their health beneﬁts
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Chapter
PHENOLIC ACIDS IN TEA AND COFFEE

AND THEIR HEALTH BENEFITS
Protiva Rani Das1,2 and Jong-Bang Eun1

1
Department of Food Science and Technology, BK 21 plus Program,
Graduate School of Chonnam National University,
Gwangju, S. Korea
2
Department of Pharmacy, University of Development
Alternative, Dhanmondi, Dhaka, Bangladesh
ABSTRACT
Tea and coffee are known to be the most popular beverages in the
world. From the ancient time tea and coffee have been consumed
intensively because of their attractive flavor and health benefits. They are
the major dietary sources of phenolic acids. Phenolic acids are aromatic
secondary plant metabolites found widely in plant based foods. Recent
interests in plant phenolic acid have drawn increasing attention due to
their high antioxidant properties and marked health benefits. Phenolic
acids have been associated with color, sensory qualities, nutritional and
antioxidant properties of foods. The relationship between the
consumption of tea and coffee and their positive health benefits might be
attributable to their phenolic acid contents. Main groups of phenolic acid
are benzoic acid derivatives such as gallic acid and cinnamic acid
derivatives such as caffeic, coumaric and ferulic acid. cinnamic acid
derivatives are higher in coffee whereas benzoic acid derivatives are
higher in tea. Chlorogenic acids (CGA) derived from caffeic acid are the
main phenolic fraction in green coffee beans. Over 30 CGA isomers are
present in green coffee beans including caffeoylquinic acids,
dicaffeoylquinic acids, feruloylquinic acid, p-coumaroylquinic acid etc.
Tea is remarkably rich in gallic acid derivatives. These phenolic acids are
2 Protiva Rani Das and Jong-Bang Eun
strong antioxidants that possess anti-carcinogenic, antitumor,

hepatoprotective, antidiabetics, antimutagenic, anti-inflammatory,
immunoprotective, hypocholesterolaemia, antidepressant, antimicrobial
and antihemorrhagic activities. 4-o-methylgallic acid in tea and isoferulic
acid in coffee are also useful as biomarkers. The main objective of this
chapter is to present an overview on the physiological effects of phenolic
acid in tea and coffee on human health. Simultaneously, the foremost
functional properties of the principle phenolic acid derivatives present in
tea and coffee are summarized, and the associated beneficial effects on
human health have been discussed in detail.
Keywords: phenolic acid, tea, coffee, health benefits
1. INTRODUCTION
Phenolic acids in general are the major classes of “phenolic compounds,”
which are composed of an aromatic ring with one or more hydroxyl groups.
Structurally when the phenol is associated with one carboxylic acid
functionality it’s referred to as “phenolic acids.” The naturally occurring
phenolic acids are distributed into two distinct groups: hydroxycinnamic and
hydroxybenzoic structure [1].
Generally, hydroxycinnamic acids are more familiar components in nature
than hydroxybenzoic acids. Mostly the plant based food contains the phenolic
acids in bound form. While, hydroxycinnamic acids rarely occurred as the free
form in plant materials. Fundamentally, it founds in foods as simplified esters
of quinic acid or glucose. On the other hand, hydroxybenzoic acids both in
free and esterified form, are found in only a few numbers of plants based foods
[2,3]. Human being can able to consume phenolic acids on daily basis owing
to their frequent presence in plant based foods. Nevertheless, tea and coffee
are considered as their major sources among various plant based foods.
Hydroxycinnamic acids are copiously presents in coffee, whereas, teas are rich
in hydroxybenzoic acids. A number of epidemiological studies have been
reported the functional properties of phenolic acids, which are related with
their enormous health benefits for humans.
Tea and coffee, in different preparations, are the widely consumed
beverages in worldwide due to their salient health benefits, attractive color and
flavor. Since ancient times, these beverages have been very well known for
their medicinal values. Coffee contains chlorogenic acid (CGA), which is the
major hydroxycinnamic acid derivative. Normally, a person consumes
Phenolic Acids in Tea and Coffee and Their Health Benefits 3
approximately 70 to 350 mg of CGA with a single cup of coffee [4, 5]. Typical
coffee consumption results in the ingestion of 0.5 to 1 g of CGA and 250 to
500 mg of caffeic acid (CA) per day [4, 6].
Furthermore, hydroxybenzoic acid such as gallic acid derivatives, are the
most abundant in tea. Tea leaves contain up to 4.5 g kg-1 fresh weight of gallic
acid [2, 7]. Among different types of teas, Chinese pu-erh teas contain the
highest amounts of gallic acid (~15 g kg-1 of dry weight) [5, 8].
The role of phenolic acids derived from tea and coffee, as dietary
antioxidants has received increasing attention in recent studies. The
antioxidant behaviors of phenolic acids are caused by the reactivity of the
phenol moiety (hydroxyl group on the aromatic ring). A number of
mechanisms are responsible for these antioxidant activities, but the
predominant mechanism is thought to be the radical scavenging activity
through hydrogen atom donation. Other important free radical scavenging
mechanisms are electron donation and singlet oxygen quenching [9]. The
hydroxyl substituent on the aromatic ring affects the stabilization as well as the
radical quenching activity of phenolic acids [1]. The biological activities of
these phenolic antioxidants are not limited to only radical scavenging and
metal chelating properties, but they are also associated with anti-carcinogenic,
anti-hypertensive, anti-diabetic, anti-microbial, hepatoprotective, anti-tumor,
neuroprotective, anti-neoplastic, anti-atherosclerotics, immunoprotective, and
anti-inflammatory activities as well as positive effects on respiratory tract
disorders and coronary heart diseases. [1, 10-15]. This chapter will review the
major phenolic acids present in tea and coffee, as well as discuss their
beneficial physiological effects on human health in detail.
2. GENERAL ASPECTS OF TEA AND COFFEE

Tea and coffee are thought to be the major components of the world
beverage market. The average coffee consumption in Asian region is
increasing around 4% per year, and the demand for coffee is predicted to
increase by 50% in this region by 2022 [16]. In addition, tea consumption has
been increasing about 4.5% to 8.8% per year from 2006 to 2011. Tea
consumption is spreading significantly across many regions like America,
Europe, Asia-Pacific and Middle East and Africa (MEA). Among them, MEA
dominated the tea market share in 2015. The tea market is expected to grow at
a compound annual growth rate (CAGR) of 4.6% during the period of 2016 to
2020 [17].
Interestingly, next to water, tea is the most consumed beverage in the

world because of its attractive aroma, good taste, and health promoting effects.
The evergreen tea comes from the “Theaceae” family and “Camelia” species.
According to Chinese mythology, tea was discovered a thousand years ago in
South-East Asia and was first cultivated in China and then in Korea and Japan.
During the 15th to 17th century when the Eastern ocean routes were opened by
the European traders, commercialization of tea was gradually expanded to
Indonesia and then to the Indian subcontinent [5, 18]. Tea is now widely
cultivated in Southeast Asia including in China, India, Japan, South Korea,
Taiwan, Sri Lanka, and Indonesia and in central African countries [19].
It is established that tea has numerous medicinal values and
pharmaceutical properties. The ancient Chinese pharmacopeia “Ben Chao
Gang mo” reported about the medicinal uses of tea. Tea is prepared by
brewing the dried leaves and buds of the plant Camellia sinensis. A number of
chemical constituents, including, polyphenols, proteins, organic matter,
minerals, free amino acids, caffeine etc. are present in tea [20]. Especially
catechins such as catechin, epicatechin, epigallocatechin gallate, gallocatechin,
and gallocatechin gallate are considered to be the main components of
polyphenols in tea [21, 22]. The chemical composition of tea differs with
variety, leaf age, climate, and season [23, 24].
Based on its processing, tea is generally classified into three different
categories: green tea (non-fermented tea), oolong tea (partially fermented tea)
and black tea (fully fermented tea) [25]. Black tea or fermented tea is produced
by promoting enzymatic oxidation of flavonoids [26]. Changes in the phenolic
compositions occur during the fermentation process [27-30] and oxidation of
the flavonols in teas gives rise to the formation of theaflavins and thearubigins.
Green tea manufacturing process involves the enzymatic deactivation, most
prominently polyphenol oxidase, which is achieved by steaming or pan frying
the fresh leaves immediately after harvesting [30, 31]. Steaming is normally
preferred in Japan, while, in China pan-frying is more common. Among the
three different types of tea, black and green teas are the main classes. About 75
to 80% of the world’s tea productions are elucidated by black tea [5, 30, 32,
33]. China, Japan and the Middle East countries prefer green tea, whereas,
oolong tea is mainly consumed in the eastern part of China, Taiwan and Japan.
In Japan the small-leaf variety of C. sinensis var. sinensis is used to produce
green tea [30, 34].
Additionally, coffee is also very popular beverages in the world after
water and tea. It is considered as one of the functional food owing to its rich
chemical composition that exerts many beneficial biological properties. Many
reasons are responsible for worldwide popularity of coffee, including its

stimulatory effects, aroma, taste, and phytochemistry [35-38]. Since the 15th
century, coffee consumption has increased tremendously. Coffee was first
cultivated in the Ethiopian region of Central Africa and then it was later
introduced in Yemen, Arabia and Egypt. From Italy coffee was first imported
into the Europe, whereas, French are known to be introducing coffee to
America. Today, more than 80 different coffee species are known worldwide.
Among them, the most common species of coffee berries are Coffea robusta
and Coffea arabica [36,39]. Consumers prefer Coffea arabica over Coffea
robusta [40]. Coffea arabica rationalizes about 75 to 80% of the World’s
coffee production and rest of 20% represents Coffea robusta. The processing
of coffee beans as a beverage involves a series of steps. After harvesting the
ripe coffee berries, it is followed by drying, roasting, grinding, and brewing to
yield the final coffee beverage. Decaffeination and filtration are additional
processing methods, which consist of the removal of caffeine and lipid
fractions. Decaffeinated coffee is predominately consumed by people with
health disorders [41]. During the last few years, at least 10% of coffee
consumption is covered by decaffeinated coffee [42-44]. During their
processing, coffee beans undergo a number of physical and chemical changes,
such as colors, flavors, and chemical constituents [36, 45, 46]. A number of
constituents are presents in coffee such as water, volatile compounds,
carbohydrates, tannins, polyphenols, proteins, caffeine, CGA, organic acids
and esters, vitamins, minerals, lipids, nitrogen compounds, and free amino
acids [47-54]. Among these various constituents, CGA accounts for the major
phenolic fraction in green coffee beans [54-58]. The basic chemical
composition of coffee mainly depends on genetic, physiological, and
processing aspects [54].
3. IDENTIFIED PHENOLIC ACIDS IN TEA AND COFFEE

3.1. Phenolic Acids in Tea
It is well known that the major polyphenols in C. sinensis are a number of

flavonols although phenolic acids and flavonoids are also present in tea [30,
59-61]. The phenolic acids found in C. sinensis tea flush are hydroxybenzoic
acids such as gallic acid, protocatechuic acid, vanillic acid, galloylquinic acid,
coumaryl quinic acid and galloylated glucose derivatives [30, 59-68]. The
structure of tea phenolic acid derivatives is given in Figure 1. Excluding
coffee, green and black tea contain high or moderate contents of phenolic
acids (30-36 mg 100g-1) [3]. Gallic acid aglycones are predominated in the
brewed tea than caffeic and p-coumaric acids. Gallic acid (3, 4, 5-trihydroxy
benzoic acid) is present in tea both as esterified or non-esterified forms. In
green tea infusions gallic acid contents range from 0.4 to 1.6 g kg-1 dry weight
[33]. Black and green tea leaves contain about 5% of gallic acid esters or free
gallic acid. Black tea contains gallic acid amounts of up to 33 m gL-1, while
green tea contains < 10 mg L-1 [30]. In fresh tea leaves, gallic acid is present
only in trace amounts [68]. However, gallic acid is not a substrate for
polyphenol oxidase, during the fermentation process the gallic acid
concentration increases which is caused by the formation of theaflavic acid by
auto oxidation process. The theaflavic acid is known to oxidize the higher
concentration of gallocatechins in fresh green leafs such as EGC and EGCG
and in the final step of these auto-oxidation processes, gallic acid is produced.
Therefore, the gallic acid production in tea depends on the degree of auto-
oxidation process [69, 70].
Catechins in tea are esterified with gallic acid to form catechin gallate
(CG), epicatechin gallate (ECG), epigallocatechin gallate (EGCG) and
gallocatechin gallate (GCG) [71]. Unesterified hydroxycinnamic acids,
including caffeic acid, ferulic acid, p-coumaric acid, mono-p-coumaroylquinic
acids, mono and di-p-coumaroylquinic acids and theogallin (1-galloylquinic
acid) are also present in teas [30, 32, 59-61, 63]. Large amounts of theogallin
and small amounts of p-coumaroylquinic acid and caffeoylquinic acids are
present in black and green tea leaves [4]. Galloylquinic acid isomers, including
3-galloylquinic acid, 4-galloylquinic acid, 1, 3, 5-trigalloylquinic acid, 4-
(digalloyl)quinic acid, 5-(digalloyl)quinic acid, and 3-galloyl-5-
(digalloyl)quinic acid or 3-(digaloyl)-5-galloylquinic acid have been identified
in green tea [5, 72]. It has been reported that [73], that most of the gallic acid
present in black tea are in non-esterified form, whereas in green tea, total
gallic acid presents as gallate esters, which contains little non-esterified gallic
acid. The identified phenolic acid derivatives in tea are summarized in Table 1.
A major gallic acid metabolite found in humans is 4-o-methylgallic acid
(4-o-MGA) [30, 74, 75]. More than 60% of gallic acid is metabolized to
4-o-MGA based on the total amount of urinary excretion [30, 76]. Other
methylated conjugates like 3-o-MGA, and 3, 4-o-diMGA is also found in urine
after ingestion of black tea [30, 73].
Figure 1. (Continued).
Figure1. Structures of identified phenolic acid derivatives in tea.

Table1. Phenolic acid derivatives in tea
Phenolic acid Sources References

1 Gallic acid C. sinensis 59-62 & 65
2 Caffeic acid C. sinensis 60 & 65
3 Ferulic acid C. sinensis 63
4 Protocatechuic acid C. sinensis 63
5 3-galloylquinic acid C. sinensis 59 & 60
8 Chlorogenic acid (5-caffeoylquinic acid) C. sinensis 59-62 & 65
9 3,5-Dicaffeoylquinic acid C. sinensis 59 & 62
10 3-p-coumaroylquinic acid C. sinensis 59 & 60
13 Vanillic acid C. sinensis 64
14 p-coumaric acid C. sinensis 60 & 65
15 1,6-digalloyl glucose C. sinensis 59
16 1,2,6-Trigalloyl glucose C. sinensis 59
17 Neochlorogenic acid (3-caffeoylquinic acid) C. sinensis 59-62 & 65
18 Cryptochlorogenic acid C. sinensis 59-62 & 65
19 Isochlorogenic acid C. sinensis 65
20 p-coumaroylquinic acid C. sinensis 65
3.2. Phenolic Acids in Coffee
Among various types of beverages coffee is the affluent sources of

phenolic acids and it contains about 97 mg of phenolic acid per 100g [3].
Many studies reported that hydroxycinnamic acids such as chlorogenic acid
(CGA), caffeic acid (CA), ferulic acids (FA), and coumaric acids, are
abundantly present in coffee. Nevertheless, CGA derivatives are the leading
phenolic acids in coffee. More than 30 CGA isomers in green coffee beans
have been characterized and identified [77]. A cup of brewed coffee (about
120 mL) contains, CGA in a range from 15 to 325 mg. As well as typical
consumption of coffee results in ingestion of 0.5 to 1 g of CGA and 250-500
mg of CA per day [6,78]. Actually, CGA in coffee is formed by comprising of
the hydroxycinnamates linked to quinic acid and finally form different
conjugated structures. Furthermore, the major CGA conjugates in coffee have

been identified as, caffeoylquinic acids (3-, 4-, and 5-o-CQA), di-
caffeoylquinic acids (3, 4-, 3, 5-, and 4, 5- diCQA), feruoylquinic acids (3-, 4-,
and 5-FQA), and p-coumaroylquinic acids, and all of them exist in several
isomeric forms [4, 13, 74, 77, 79, 80-83]. Among them, 5-CQA is considered
as the predominant isomer. The structures of coffee phenolic acid derivatives
are given in Figure 2. In green coffee beans, CQA and diCQA account for
84% of the total phenolic contents [84]. Commercial green coffee beans
contain higher concentrations of CGA isomers especially 5-CQA than the
immature green coffee beans [79]. Additionally, coffee contains caffeoylquinic
acid lactones (CQAL) [81] and protocatechuic acid (3, 4-dihydroxy benzoic
acid) [85, 86]. The identified phenolic acid derivatives in coffee are listed in
Table 2. The major CGAs in green coffee extract present in a ratio of CQA,
FQA, and di-CQA (70:19:11) [87]. The ratio of these CQA isomers is
22:27:51 for 3-CQA, 4-CQA and 5-CQA respectively. Isoferulic acid is used
as a biomarker for coffee derived polyphenol exposure [74].
OH
O
OH
OH
OH
HOOC
HOOC O
OH
OH O OH OH
OH
OH
O
3-0-caffeoylquinic acid 4-0-caffeoylquinic acid
OH
OCH3
OH
OH
OH
HOOC
O OH
O
OH O
5
HOOC
OH
O
OH OH
5-0-caffeoylquinic acid 3-0-feruoylquinic acid
O
O
OH
HOOC O
O
HOOC
OH
OH OH OH
OH
OH OH
OMe
OMe
4-0-feruoylquinic acid 5-0-feruoylquinic acid
OH
HOOC
O
3 OH
OH 4
OH O
O HOOC O
OH OH
OMe
OMe
OMe
OMe
3-0-dimethoxycinnammoylquinic acid 4-0-dimethoxycinnammoylquinic acid
OMe OH OH
HO OH
OMe
OH
O
HOOC O O
HOOC OH
O OH O
O OH O
O
HOOC OH
OH OH
OH OH
OH OH
5-0-dimethoxycinnammoylquinic acid 3,4-di-0-caffeoylquinic acid 3,5-di-0-caffeoylquinic acid
OH
OH
MeO
OMe
OH
OH
OH
O
HOOC O O
O HOOC OH
O OH O
O OH O
O
HOOC O
OH OH
OH OMe
OMe
OH OH
OH
4,5-di-0-caffeoylquinic acid 3,4-di-0-feruloylquinic acid 3,5-di-0-feruloylquinic acid
OH
OH OH
MeO
HO
OMe
OH
OH
HOOC O O
O HOOC O O
OH O
O OH O
O
O
HOOC O
OH OH
OH OMe OH
OH OH
OMe
4,5-di-0-feruloylquinic acid 3-0-feruoyl, 4-0-caffeoylquinic acid 3-0-caffeoyl, 4-0-feruloylquinic acid
3-0-feruloyl, 4-0-dimethoxycinnammoylquinic acid 3-0-dimethoxycinnammoyl, 5-0-feruloylquinic acid
OMe
OMe
OMe
OH
O
O
HOOC OH O
OH O
O
O
HOOC O
OH OH
OMe
OMe
OMe
OH
3-0-feruloyl, 5-0-dimethoxycinnammoylquinic acid 4-0-dimethoxycinnammoyl, 5-0-feruloylquinic acid
OMe OH
OMe
OH
O
O
OH
O
O
O OH O
HOOC O
OH OH O
OH
OMe
4-0-feruloyl, 4-0-dimethoxycinnammoylquinic acid 3-0-caffeoylquinic acid lactone
OH
OH
OH
O OH
O
O O
HOOC
OH OH O
OH OH O
4-0-caffeoylquinic acid lactone 4-0-p-coumayolquinic acid

16 Protiva Rani Das and Jong-Bang
4-0-caffeoylquinic acid lactone Eun
4-0-p-coumayolquinic acid
OH
HO
O
OH
HO
HOOC O
OH
OH OH O
5-0-p-coumayolquinic acid Caffeic acid
OH
HOOC OH
O O OH
O
OH
HO
OCH3
OMe
OMe
Ferulic acid 1-0-dimethoxycinnamoylquinic acid
Figure 2. Structures of identified phenolic acid derivatives in coffee.
Table2. Phenolic acid derivatives in coffee’

1 3-o-caffeoylquinic acid C. robusta, C. canephora [77, 79 & 81]
var. robusta
2 4-o-caffeoylquinic acid C. robusta,C. canephora [77, 79 & 81]
var. robusta
3 5-o-caffeoylquinic acid C. robusta, C. canephora [77, 79, 81, &
var. robusta 82]
4 3-o-feruoylquinic acid C. robusta [77 & 81]
5 4-o-feruoylquinic acid C. robusta [77 & 81]
6 5-o-feruoylquinic acid C. robusta, C. canephora [77, 79 & 81]
var. robusta
Table 2. (Continued)

7 3-o-dimethoxycinnammoylquinic acid C. robusta [77]
10 3,4-di-o-caffeoylquinic acid C. robusta, C. canephora [77, 79 &
var. robusta 81]
var. robusta 81]
var. robusta 81]
13 3,4-di-o-feruloylquinic acid C. robusta [77]
16 3-o-feruoyl, 4-o-caffeoylquinic acid C. robusta [77]
17 3-o-caffeoyl, 4-o-feruloylquinic acid C. robusta [77]
18 3-o-feruloyl, 5-o-caffeoylquinic acid C. robusta [77]
19 3-o-caffeoyl, 5-o-feruloylquinic acid C. robusta [77]
20 4-o-feruloyl, 5-o-caffeoylquinic acid C. robusta [77]
21 4-o-caffeoyloyl, 5-o-feruloylquinic acid C. robusta [77]
22 3-o-dimethoxycinnammoyl, 4-o- C. robusta [77]
caffeoylquinic acid
23 3-o-caffeoyl,4-o- C. robusta [77]
dimethoxycinnammoylquinic acid
24 3-o-dimethoxycinnammoyl,4-o- C. robusta [77]
caffeoylquinic acid
26 4-o-dimethoxycinnammoyl,5-o- C. robusta [77]
caffeoylquinic acid
feruloylquinic acid
29 3-o-feruloyl, 4-o- C. robusta [77]
feruloylquinic acid
31 3-o-feruloyl, 5-o- C. robusta [77]
32 4-o-dimethoxycinnammoyl, 5-o-feruloylquinic acid C. robusta [77]
33 4-o-feruloyl, 4-o-dimethoxycinnammoylquinic acid C. robusta [77]
34 3-o-caffeoylquinic acid lactone coffee [81]
35 4-o-caffeoylquinic acid lactone coffee [81]
36 4-o-p-coumayolquinic acid coffee [81]
37 5-o-p-coumayolquinic acid coffee [81]
38 Caffeic acid coffee [82]
39 Ferulic acid coffee [82]
40 1-o-dimethoxycinnamoylquinic acid C. robusta [77]
4. HEALTH SIGNIFICANCE OF PHENOLIC ACID

DERIVATIVES IN COFFEE AND TEA
4.1. Health Benefits of Phenolic Acids in Coffee
4.1.1. Antidiabetic Activity

The relationship between coffee consumption and a reduction in the risk
of diabetes mellitus (DM), especially type 2 diabetes mellitus (T2DM), has
been reported by a number of authors. Among various health benefits, the
major coffee CGAs exert the antidiabetic effects is the most prominent.
Glucose and lipid metabolic disorders are related to the development of
diabetes. The role of coffee’s phenolic acid, especially CGAs, and their
application in glucose and lipid metabolism has been reported [13]. Many
other natural resources for diabetes prevention exist, and among them, coffee
CGA is potential components for the reduction of diabetic’s risk [88].
Noticeably, coffee consumption reduces the risk of T2DM due to the
presence of principle coffee constituents such as CGA [89-96]. CGA exhibited
antidiabetic potential at a dose of 5 mgkg-1 bodyweight in streptozotocin-
nicotinamide (45 mgkg-1 bodyweight) induced diabetics in rats [97-99]. Some
studies demonstrated that coffee CGA exerts effects similar to metformin [95]
rosiglitazone, thiazolidinedione or insulin and can overcome the side effects
associated with these synthetic medications [100] and the antidiabetic activity
of CGA against T2DM has also been confirmed by clinical trials [101].
Daily consumption of 3 to 4 cups of coffee is associated with a 25%
decreased risk of T2DM and consumption of more than 3 to 4 cups of
decaffeinated coffee reduces the risk of T2DM by approximately 30% due to
their higher content of CGA [102]. The effects of decaffeinated coffee extracts
and their major components on glucose and insulin concentrations were
evaluated by oral glucose tolerance test (OGTT) [103]. The results showed
that CGA significantly reduced the early fasting glucose and insulin responses.
CGA in coffee has the ability to modulate plasma glucose uptake, insulin and
gastrointestinal hormone secretion [104]. The antidiabetic activity of coffee
extract showed that coffee consumption prevents the T2DM [105]. Coffee
extracts work by inhibiting both recombinant and endogenous 11ᵝ-
hydroxysteroid dehydrogenase type 1 (11ᵝ-HSD1) activity in a liver cell
model, which results in a decrease in gluconeogenesis. Coffee extract inhibited
11ᵝ-HSD1-dependent cortisol formation, nuclear translocation of
glucocorticoid receptor and glucocorticoid-induced expression of
phosphoenolpyruvate carboxykinase. The authors group suggested that, the
antidiabetic activity of coffee extract was due to the inhibition of 11ᵝ-HSD1-
dependent glucocorticoid reactivation.
A number of epidemiological studies showed that coffee consumption
reduced the risk of T2DM by suppressing excess fat accumulation in
adipocytes. The effects of roasted and green coffee bean extracts on the
differentiation of mouse preadipocyte 3T3-L1 cells and on PPARy-target
genes which are involved in glucose metabolism was investigated [106]. Both
coffee extracts reduced the accumulation of lipids during adipocytic
differentiation and inhibited the expression of PPARy gene. Moreover, coffee
extracts reduced the expression of other differentiation marker genes, aP2,
adiponectin, CCAAT-enhancer-binding protein α (C/EBPα), glucose
transporter 4 (GLUT4), and lipoprotein lipase (LPL) during adipocyte
differentiation. CGA and CA significantly inhibited the enzymes which are
involved in lipid metabolism such as fatty acid synthase, 3-hydroxy-3-
methylglutaryl CoA reductase and acyl-CoA/cholesterol acyltransferase [107].
There are many mechanisms suggested for how to CGA acts as an
antidiabetic agent including α-glucosidase inhibition, α-amylase inhibition,
glucose-6-phosphatase (G-6-Pase) inhibition, Adenosine Monophosphate
Activated Protein kinase (AMPK) activation, improvement of cellular
mechanism, regulation of glucose-dependent insulinotropic peptide (GIP)
concentration, and upregulation of hepatic PPAR- α expression etc.
Some of the major possible mechanism of coffee CGA action in diabetics
is described below:
4.1.1.1. α-glucosidase and α-amylase Inhibition

α-glucosidase helps to breakdown the complex carbohydrates into
glucose, whereas α- amylase hydrolyzes the alpha bonds of complex
polysaccharides to yield glucose and maltose. Acarbose, voglibose and
miglitol are synthetic α-glucosidase and α–amylase inhibitors. It has been
reported that CGAs act as an antidiabetic agent by inhibiting α-glucosidase
and α- amylase activity. The effect of coffee consumption on human was
examined by glucose tolerance test [108] and the authors found that coffee
consumption can reduce the raising plasma glucose concentration due to their
CGA content. It has been suggested that CGAs in coffee exerted the
antagonistic activity on glucose transport. Coffee seeds hot water extract on
the postprandial blood glucose concentration in rats by oral saccharinity
tolerance test (OST) has been investigated [109]. The inhibitory activity of
coffee extract was investigated both in in vivo and in vitro against α–
glucosidase and α–amylase. The authors reported that CGAs in coffee act as
acarbose by strongly inhibiting the activity of α–glucosidase and α–amylase
thus resulting in a reduction of the postprandial blood glucose concentration.
Other studies showed that a CGA derivative can inhibit the intestinal α–
glucosidase activity by reducing the postprandial blood glucose level in an
uncompetitive manner and its activity was similar to that of acarbose, migitol
and voglibose [110-112]. CGA and its isomers from coffee beans showed
inhibitory activity against porcine pancreas α–amylase (PPA) isozymes PPA-I
and PPA-II [113, 114]. It has been reported that, decaffeinated coffee extracts
possess antidiabetic activity [79]. The authors of this report strongly suggested
that the mechanism of anti-hyperglycemic activity of coffee extracts was due
to the inhibition of intestinal α–glucosidase by CQAs, FQAs, and di-CQAs.
4.1.1.2. AMPK Activation

AMP activated protein kinase (AMPK) is a main sensor that maintains
and regulates the cellular energy homeostasis [115,116]. Normally, a number
of stimulatory factors are involved in activation of AMPK such as
pharmacological, pathological and metabolic agents including metformin,
thiazolidinedione, hypoxia, and exercise. Finally the activated AMPK, induces
the transfer of GLUT4 (glucose transporter type 4) from intracellular
membrane to plasma membrane thus resulting in increasing glucose transport.
CGAs can induce the regulation of glucose transport in skeletal muscle
isolated from (db/db) mice and L6 skeletal muscle cells through the activation
of AMPK [117]. The authors of this study showed that, CGA stimulated
glucose transport in a time and dose dependent manner. Similarly, other
reports [118, 119] found that, CGA enhanced glucose uptake through
increasing GLUT4 expression. The effects of CGA on glucose tolerance,
insulin sensitivity, hepatic gluconeogenesis, lipid metabolism, and skeletal
muscle glucose uptake in Leprdb/db mice were examined [120]. The result
showed that CGA activates AMPK, which is associated with beneficial
outcomes, such as reduction of hepatic glucose production and fatty acid
synthesis. Finally the authors concluded that, CGA improved glucose and lipid
metabolisms through AMPK activation. CGA can also increases the mRNA
levels of GLUT4 in STZ-induced diabetic rats [121].
4.1.1.3. Inhibit the Expression of G-6-Pase

Glucose 6 phosphatase (G-6-Pase) hydrolyzes the glucose 6-phosphate
and then resulted in gluconeogenesis and glycogenesis. Finally, glucose is
formed from gluconeogenesis [122]. Many reports showed that, CGA has
beneficial effects on glucose absorption and that can improve systematic
glucose control [93, 100, 121, 123-125]. The two major pathways responsible
for the release of glucose from the liver include G-6-Pase activation and
increases in blood glucose concentration [101, 126-129]. CGA derivatives can
delay intestinal glucose absorption by inhibiting glucose-6-phosphate
translocase and reducing sodium gradient driven apical glucose transport [125-
126]. The major phenolic acids in coffee, CGAs (especially CQA and di-
CQA) showed inhibition of G-6-Pase hydrolysis thus resulting in glucose
lowering effects by reducing hepatic glucose production [130]. CGA inhibited
40% of G-6-Pase activity in the microsomal fraction of hepatocytes [93].
Consequently, CGA inhibited G-6-Pase thus resulting in reduced hepatic
glucose output [118,125, 126, 131]. Furthermore, CGA can act as an active
fundamental in the glucose metabolism principle [12, 119,132].
The interaction of CGA and 2-hydroxy-5-nitrobenzaldehyde with rat
hepatic G-6-Pase has been investigated [125]. Results showed that both of
them are competitive inhibitor of G-6-Pase hydrolysis. This study also
reported that CGA can selectively bind to T1 (G-6-pase transporter). Whereas,
the inhibition of T1 results in selectively obstruct the G-6-pase transporter.
CGAs showed antidiabetic activity in STZ-induced diabetic rats through the
inhibition of G-6-Pase [133]. CGA has effects on hepatic-6-Pase, skeletal
muscle GLUT4 expression, blood glucose and lipid levels in STZ-induced
diabetes in rats [121]. The result showed that CGA exhibited effects on
improving blood glucose, inhibition of G-6-Pase, changes in glucose
metabolism, lipid metabolism, and insulin sensitivity. CGA can improve the
glucose/lipid metabolism in db/db mice by inhibiting the G-6 Pase [134].
The antidiabetic effect of ferulic acid (FA) was demonstrated by a number

of studies [135-140]. The mechanism of the antidiabetic properties of FA
includes the ability to inhibit α–glucosidase [136], porcine pancreatic α-
amylase isozyme [110], and increased expression of GLTU4 and P13K genes
[30].
4.1.2. Cardiovascular Activity

The leading causes of global death are known to be caused by
cardiovascular disease (CVD). Among many contributing factors,
hypercholesterolemia is the major risk factor for the development of CVDs.
Usually a number of agents are used to treat CVDs. Coffee’s major
constituents CGAs are one of them.
Oxidative modification of low density lipoprotein (LDL) by free radicals
plays a key role in the early stage of atherosclerosis [13]. The rapid uptake of
LDL, modified through oxidation by a receptor leads to the formation of foam
cells. Oxidized LDL is also associated with a number of atherogenic properties
[141]. The coffee major phenolic acid, CGA can reduce cardiovascular risk by
quietly reducing LDL oxidation susceptibility and LDL cholesterol levels
[142]. The in-vivo studies of coffee consumptions on healthy humans are
reported [143]. Their results exerts that the coffee consumption significantly
reduced LDL cholesterol, serum levels of total cholesterol and
malondialdehyde levels (MDA). Their study suggested that, CGAs in coffee
can favorably effects CVDs by reducing LDL oxidation susceptibility and
decreasing LDL-cholesterol and MDA levels. Coffee CGA has effects on
hyperlipidemic and insulin resistant (fa/fa) Zucker rats [10]. An in vivo study
in these rats showed that, CGA can improve glucose tolerance, decrease
plasma and liver lipids and improve mineral pool distribution. CGA can
significantly reduce the concentration of cholesterol and triacylglycerol by
44% and 58% respectively, as well as the liver triacylglycerol concentration
(24% reduction). Dietary CGA significantly reduced the plasma total
cholesterol level and LDL in a dose dependent manner [144]. This study
investigated the effects of CGA by monitoring the plasma lipid profile in rats.
As well as, the authors found that, lipid accumulations were significantly
decreased in hypercholesteremic animals through CGA supplementation. The
hypocholesterolemic activity of CGA is mainly due to the increased level of
fatty acid utilization in the liver via the upregulation of peroxisome
proliferation activated receptor α-mRNA. Consequently, the
hypercholesterolemic effects of CGA lead to the atheroscleroprotective,
cardioprotective, and hepatoprotective properties.
Green coffee bean extracts (GCBEs) and their main constituents effects on
mice have been investigated [145]. Their results exhibited that the GCBE
reduced visceral fat content and body weight due to their phenolic acids. Both
0.5% and 1% GCBE reduced visceral fat content and body weight. The
authors of this study suggested that the phenolic acid derivatives in GCBE are
effective against weight gain and fat accumulation. About 200 ml (1 cup) of
coffee induces an increase in the resistance of LDL to oxidative modification
because of the coffee phenolic acids are incorporated into LDL [146]. The
CGAs from green coffee bean extract (GCE) have blood pressure lowering
effects and safety effects with mild hypertensive patients [87]. The inhibitory
activity was investigated through a placebo-controlled, randomized clinical
trial. These group of researchers found that CGA from GCE was able to
effectively decrease blood pressure in a safe manner. Another study also
reported that CGA from water-soluble green coffee bean extract (GCE) have
hypotensive effect [147]. The authors group reported that, 5-CQA, the major
component of GCE showed dose dependent blood pressure lowering effects in
hypertensive rats. The authors suggested that, 5-CQA and FA (metabolite of 5-
CQA in humans) are potential hypotensive candidates. The authors
demonstrated that, the short-term ingestion of GCE in humans has a
hypotensive effect and reported a dose-response relationship from 70 mg to
280 mg CGA per day.
4.1.3. Anticancer Properties

It is already reported by a number of studies that phenolic acids in coffee
exert potential antioxidant properties that are associated with anti-cancer
activities. Coffee phenolic antioxidants exhibited the anticancer activity in
both in-vivo and in-vitro studies [79, 84, 148-158].
Normal cell transformed to cancerous cell depends on the formation of
several stimulatory factors which is induced due to the accumulation of
multiple mutations provided by genomic instability. Genomic instabilities are
caused by increased amounts of mutagens and an insufficient DNA integrity
control system such as cell cycle check points control tools or DNA-repair
machineries [7]. Seven hydroxycinnamic acid derivatives, 3-caffeoylquinic (3-
CQA), 4-caffeoylquinic acid (4-CQA), 5-caffeoylquinic acid (5-CQA), 5-
feruoylquinic acid (5-FQA), 3,4-dicaffeoylquinic acid (3,4 diCQA), 3,5-
dicaffeoylquinic acid (3,5 diCQA), and 4,5-dicaffeoylquinic acid (4,5 diCQA)
were isolated from low quality (immature) and commercial green coffee beans
(C. canephora var. robusta) [79]. These isolates exhibited antioxidant,
antiproliferative, and tyrosinase inhibitory activities. Among them diCQAs
showed stronger free radical and superoxide anion radical scavenging activity
than FQA, CQA, CA and commonly used antioxidants such as α-tocopherol
and ascorbic acid did. di-CQA also exhibited more potent tyrosinase inhibitory
activity compared to 5-CQA, arbutin and ascorbic acid (usual tyrosinase
inhibitors). Tyrosinase activity was estimated by measuring the amount of
dopachrome produced from L-tyrosine and L-DOPA by tyrosinase. di-CQA
inhibited the formation of dopachrome by about 45 to 50% and that of L-
DOPA by about 51 to 59%. Antiproliferative activities of these isolates were
studied in four human cancer cell lines such as, human histolytic lymphoma
U937, human oral carcinoma KB, human breast carcinoma MCF7, and SV40
virally transformed W138-VA. The IC50 value was ranged from 0.10 to 0.56 m
for the KB cells, which was the most sensitive cell line among these cultured
cells. di-CQAs exhibited the most potent antiproliferative activities at lower
IC50 compared to FQA and CQA. Methyl esters of diCQAs and triCQA have
antiproliferative activity against murine colon 26-L5 carcinoma, human lung
carcinoma A-549, human HT-1080 and murine B16-BL6 melanoma at lower
IC50 values [159]. The authors of this study finally concluded that,
hydroxycinnamic acid derivatives especially diCQAs from both green coffee
beans can act as useful chemopreventive agents, anti-oxidants and skin
whitening agents. Additionally, a number of other studies reported that, 5-
CQA and di-CQAs showed inhibitory activity against the proliferation of
carcinogenic cells and neoplastic transformation of epidermal cells reduced the
lipopolysaccharide-induced inflammation in macrophages and inhibited the
expression of cyclooxygenase 2 and different pro-inflammatory mediators
[160-164].
Coffee phenolic acids possess potential anti-genotoxic activity against
severe carcinogenic mice [152, 153], bacterial strains [155-157] and
drosophila [154]. The major coffee phenolic acid like CGA and FA have
inhibitory effects on development of aberrant crypt foci (ACF) in colorectal
carcinogenesis in rats [150, 151] while, ACF is considered as potential
precursor lesions for colorectal cancers in rodents and humans. These group of
study suggested that, CGA and FA can be used as promising agents for
preventing human colorectal cancers. It has been reported that, long term
coffee consumption showed inhibitory effects on nitrosamine-induced
hepatoprotective carcinogenesis in rats [165]. The authors reported that, the
major coffee phenolic acid, CGA showed the inhibitory activity against
chemical carcinogenesis in liver. Furthermore, CGA was able to inhibit the
methylazoxymethanol acetate-induced large bowel carcinogenesis in hamsters
and prevent 4-nitroquinolone 1-oxidase –induced oral carcinogenesis in rats

[166, 167].
Coffee consumption has modulatory effects on transplacental genotoxicity
induced by cyclophosphamide (CPH), N-nitrosodoetylamine (DEN), N-nitro-
N-ethylurea and mitomycin C (MMC) in Swiss albino mice [158]. A
transplacental micronucleus test showed that, coffee administration
significantly inhibited the effects of CPH, DEN, ENU, and MMC in fetal liver
and fetal blood due to their major phenolic acids. The synergistic effects of
coffee consumption and dietary constituents against genotoxicity induced by
genotoxins were examined in another study [168]. Co-administration of coffee
with dietary constituents such as, CGA, FA and CA enhanced the anti-
genotoxic effects compared with either coffee or dietary constituents alone.
The authors also suggested that, normal level of coffee consumption have
beneficial health effects. The dose of 250 to 500 mg coffee kg-1 body weight
showed significant in-vivo anti-genotoxic effects in mice [153, 169].
In cellular communication reactive oxygen species (ROS) play important
roles by regulating biological processes including inflammation, proliferation,
and cell differentiation. While, ROS are beneficial for several cellular
mechanisms but, excess amounts of ROS can damage cells and result in DNA
mutations or lipid and protein oxidation [170]. In-vitro activities of different
concentration of green coffee bean extract (GCBE) and its major phenolic
acids, such as 5-CQA and 3, 5-DCQAs for treating human HepG2 cells is
reported [84]. These phenolic acids significantly give protection against
oxidative stress induced by tert-Butyl hydroperoxide (t-BOOH). The authors
of this study showed that, GCBE and its major phenolic acids can potentially
defend cells against oxidative damage by modulating cell-cytotoxicity, ROS
generation, antioxidant activity and macromolecular damage.
The effect of coffee consumption on 1,090 patients with invasive primary
breast cancer has been examined [171]. The clinical experimental findings
demonstrated that the CA in coffee reportedly showed anticancer properties
against two breast cancer models. CA and caffeine can suppress the growth of
tumor cells and results in reduction of breast cancer. Several other studies also
reported the activity of coffee phenolic acid against breast cancer [172-174].
Due to its major phenolic acid contents, daily consumption of more than five
cups of coffee can reduce the risk of breast cancer by 50% compared to
drinking two cups. Instant caffeinated coffee (ICC) and CA have also been
investigated for their anticancer activity [175]. ICC and CA were able to
significantly reduce the expression of cyclin D1 in breast cancer cells through
the modulation of STAT5B and ATF-2. Cyclin D1 expression regulation has
an effective role in the treatment of human neoplasms, which has also been
reported by other authors [176-179].
The inhibition of CT-26 colon cancer cell-induced lung metastasis by
blocking phosphorylation of ERKs in human samples was found by phenolic
acid in coffee such as CGA and CA [180]. The authors group also reported
that, CA can directly bind and inhibit MEK1 and TOPK activities, which are
known as upstream activators of ERK in an ATP non-competitive manner.
These results suggested that, coffee phenolic acid inhibits ERKs
phosphorylation and target MEK1 and TOPK to suppress the colon cancer
metastasis and neoplastic cell transformation.
Coffee CGA derivatives have inhibitory activities on DNA
methyltransferase 3a (Dnmt3a), an enzyme that is associated with the
development of cancer [181]. Among 12 CGA derivatives seven showed
inhibitory activity against Dnmt3a. This authors group suggested that 1,-3-
dicaffeoyl-muco-quinic acid diacetal can act as a leading compound due to
their potential inhibitory activity. CA in coffee exhibited anti-proliferative and
anti-invasive activity in both in-vivo and ex-vivo studies [182]. When instant
coffee powder was added directly to the culture media it exhibited the
proliferation and invasion inhibitory activity in rat ascites hepatoma cell line
AH109A. The authors attributed that, this anti-invasive action of CA into its
free radical scavenging activity.
Moderate coffee consumption had lower risk of colon cancer in
postmenopausal women [183]. The authors studied the effects of coffee on
estrogen sulfotransferase (SULT) because the sulfation pathway plays a major
role in estrogen inactivation. Coffee consumption resulted in 60% reduction of
SULTIEI gene expression in caco-2 cells. The ability of coffee consumption to
reduce cancer incidence was confirmed by a meta-analysis report [184].
Consumption of coffee and its major constituents, CGA shows inhibitory
activity against hepatocellular carcinogenesis [167]. An aqueous extract of C.
arabica showed higher anti-oxidant and anti-inflammatory activities than the
reference sample did owing to their presence of polyphenolic compound
especially CGA [185]. The effects of two different types of coffee blends
(CGA and trigonelline-rich market blend (MB) and N-methylpyridinium rich
syudy blend (SB) with known composition on inflammatory gene transcription
in 84 healthy human peripheral blood lymphocytes were investigated [186].
The authors group concluded that, regular consumption of coffee affects
transcription factors of genes which are associated with inflammation and
obesity. Coffee consumption significantly decreased the transcription of the
Nrf2, peroxisome-proliferator activated receptor y (PPARy), and pro-
inflammatory interleukin 6 (IL6). The authors group concluded that, MB

coffee blends contain higher amounts of the transcriptional factor lowering
compounds than SB coffee. This anti-inflammatory effect was correlated with
the presence of different CGA metabolites. Coffee constituents like CGA (5-o-
caffeoylquinic acid) were identified as inducers of the Nrf2/antioxidant-
response element (ARE) detoxifying pathway under cell culture condition that
induces the chemopreventive enzymatic activity in both in-vivo and in-vitro
studies [187, 188]. Further, lipoxygenase inhibitory activity was exerted by
CA [189].
4.1.4. Antimicrobial Activity
Coffee phenolic acid possesses antimicrobial activity against both gram-
positive and gram-negative bacteria, which has been reported by a number of
authors [85, 190-199]. The antibacterial activity of coffee beverages against
cell growth and biofilm formation of Streptococcus mutans was determined
[190]. Generally, S. mutans is a carcinogenic bacterium. This study aimed to
identify the chemical compounds from coffee that exerted the antibacterial
activity. Aqueous extracts of green and roasted regular and decaffeinated
coffee from C. arabica and C. canephora beans were tested. Their results
indicated that, 5-CQA and CA solutions showed bacteriostatic activity and
their minimum inhibitory concentration (MIC) value was 0.8 mg mL-1.
Comparatively,
C. canephora beans showed more biofilm formation inhibitory activity than
C. arabica beans.
Brewed coffee showed antibacterial activity against pathogenic Legionella
pneumophila [85]. In this study, active fractions from coffee extracts were
isolated by using HPLC, NMR and LC-mass spectrometry. Protocatechuic
acid (3, 4-dihydroxy benzoic acid), CGA and CA were identified as the
antibacterial compounds.
The ability of green and roasted coffee extracts (from C. arabica and C.
robusta) to interfere with S. mutans sucrose-independent adsorption to saliva-
coated hydroxyapatite (HA) beads was analyzed [191]. The inhibition of S.
mutans adsorption to the HA beads was observed when coffee was present in
the absorption mixture and when it was used to pretreat the beads. The authors
of this study proposed that, the theory of antibacterial activity of coffee
components especially CGA may adsorb to a host surface resulting in the
prevention of tooth receptor from the interaction with any bacterial adhesions.
Phenolic acids from C. canephora extract showed in-vitro antibacterial activity
against S. mutans and S. sobrinus which are responsible for dental carries
[192]. These authors also suggested that, coffee extract acts against dental
carcinogenesis. Coffee extracts from C. arabica and C. robusta showed

potential activity against S. aureus due to their CGA components [193,194].
Roasted coffee beans possess antibacterial activity against enterobacteria. The
effects of commercial coffee bean extracts against nine strains of
enterobacteria were determined [86]. Both CGA and protocatechuic acid
showed strong activity against Serratia marcesens and Enterobacter cloacae.
CA also showed inhibitory activity. The authors concluded that,
protocatechuic acid can be used as a potential agent against Salmonella
enterica. The antimicrobial activity of green coffee CGAs against different
bacterial strains (B. cereus, C. sporogenes, L. innocua, M. luteus, S. aureus, E.
coli, P. fluroscens, and S. enterica), fungi (A. flavus and A. ochracus) has been
determined [200]. CGA exhibited antibacterial activity against both gram-
positive and gram-negative bacteria. It exhibited bactericidal activity against
P.fluorescens and S. aureus and presented anti- aspergillus activities and anti-
mycotoxigenic activity against A.ochratoxin. Health benefits of phenolic acids
isolated from coffee sources are summarized in Table 3. Moreover, coffee’s
CGA also possessed antiviral activity. Coffee consumption can provide
protection from AIDS which is caused by HIV virus [201-203]. Certain
diCQAs and caffeoylmalic acid showed antiviral activity by interfering with
the metabolism of HIV-1 in cultured cells.
Table 3. Summary of the health benefits of coffee phenolic acids
Coffee Phenolic acid Heath benefits References

C. canephora var. di-caffeoylquinic acids Anticancer [79]
robusta (di-CQAs)
Coffee bean extract CGA, FA Anticancer [150 &
166]
Coffee powder Major phenolic acids Anticancer [158]
Coffee powder CGA, FA, caffeic acid Anticancer [168]
Coffea arabica 5-CQA, 3,5 diCQA Anticancer [84]
Coffee Caffeic acid Anticancer [171]
Commercial instant CGA, Caffeic acid Anticancer [6]
coffee
Coffee 1, 3-dicaffeoyl-muco-quinic Anticancer [178]
acid diacetal
Instant coffee powder Caffeic acid Anticancer [181]
Instant caffeinated Caffeic acid Anticancer [175]
coffee
Arabica coffee Phenolic acid Anticancer [183]
Coffee Phenolic acid Anticancer [184]
C. Arabica & CGA, CA Antimicrobial [190]

C. canephora
Brewed coffee extract Protocatechuic acid (3, 4- Antimicrobial [85]
difydroxy benzoic acid),
CGA and caffeic acid
Coffea arabica Protocatechuic acid, CGA, Antimicrobial [86]
Caffeic acid
Coffea canephora Phenolic acid Antimicrobial [191]
C. arabica & CGA Antimicrobial [191]
C. robusta
C. arabica & Phenolic acid Antimicrobial [193]
C. robusta
Coffee Phenolic acid Heath benefits References

Coffea arabica Caffeic acid, protocatechuic Antimicrobial [194]
acid & CGA
Coffee CGAs Antimicrobial [200]
Instant coffee CGA Antidiabetic [104]
Coffee extract CGA Antidiabetic [109]
Decaffeinated green CGAs Antidiabetic [113]
coffee bean extracts
Coffea arabica Major coffee compounds Antidiabetic [105]
Coffea canephora CGA, CQA, di-CQA Antidiabetic [130]
Coffea canephora CQAs, FQAs, di-CQAs Antidiabetic [79]
Arabica coffee CGA Cardioprotective [143]
Coffea canephora CGAs Cardioprotective [145]
Coffee CGA Cardioprotective [146]
Green coffee bean CGA Cardioprotective [87]
Green coffee bean 5-CQA, FA Cardioprotective [147]
4.2. Health Benefits of Tea Phenolic Acids
4.2.1. Anti-Diabetic Activity

Teas are a very popular nutraceutical owing to their anti-oxidant activities
as well as antidiabetic properties. Particularly, green tea possesses anti-obesity
and antidiabetic properties [201]. Gallic acids in tea are well known compound
for the treatment of diabetes [205-210]. Sri-Lankan traditional practitioner
uses black teas for diabetes treatment which reduces diabetes through
increasing diuresis. Black tea infusion (BTI) showed diuretic effects in a study
using rats [211]. The results from this study indicated that, the BTI
significantly induced diuresis in a dose dependent manner. The study also

discusses a number of mechanisms for the diuretic activity of BTIs, such as
inhibition of both aldosterone secretion and carbonic anhydrase, via a thiazide
type mechanism due to their phenolic contents. The anti-hyperglycemic
activity of oolong tea on patients with T2DM has been determined [212].
Results showed that oolong tea is very effective in lowering T2DM. As well
as, this lowering effect was due to the polyphenols present in tea including
gallic acid.
Figure 3. Overview of the mechanisms of action of phenolic acids of coffee and

tea on diabetes. (C/EBPα: CCAAT-enhancer-binding protein α; FAS- fatty acid
synthase; GLUT4: glucose transporter 4; G6Pase: glucose-6-phosphatase; HMG-
CoA reductase: 3-hydroxy-3-methylglutaryl coenzyme A reductase; INS: insulin
gene; PDX-1: pancreatic and duodenal homeobox 1; PEPCK:
phosphoenolpyruvate carboxykinase; P13K: phosphatidylinositol-3-kinase; PPAR-
peroxisomal proliferator-activated receptor).
The antidiabetic mechanism of gallic acid has been described in detail

[205]. Basically, gallic acid induces GLUT4 translocation and glucose uptake
activity in 3R3-L1 cells. For glucose transportation GLUT4 protein needs to
translocate from the intracellular pool to the plasma membrane. The GLUT4
transportation plays an important role for glucose transport in muscle and
adipocytes. It is thought that, certain compounds are able to enhance this
process. Gallic acid is one of compound that showed increased GLUT4
translocation and glucose uptake activity. Generally, it has been shown that
GLUT4 translocation and glucose uptake are mediated by two major pathways
such as an insulin dependent AMPK pathway and an insulin mediated P13K
pathway. The authors group in this study found that gallic acid induces
glucose uptake in a P13K dependent manner but not through the activation of
AMPK. A similar report was showed that, gallic acid can prevent STZ-
induced hyperlipidemia, hypertension, and bradycardia [206]. As well as,
structural alterations in cardiac tissue such as, an increase in force of
contraction, left ventricular weight to body weight ratio, collagen content,
serum lactate dehydrogenase and creatinine kinase levels were prevented by
gallic acid in a dose depended manner. This report suggested that gallic acid
could be used for the treatment of myocardial damage associated with type 1
diabetes. Other studies reported that gallic acid reduced oxidative stress in
STZ-induced hyperglycemic rats. The mechanism of STZ-induced pancreatic
β–cell toxicity was reduced by gallic acid due to its free radical scavenging,
anti-lipid peroxidation and antioxidant activities that protect β–cells, resulting
in increased plasma insulin concentration and decreased blood glucose levels
[213-215]. Importantly, pancreatic β–cell protection is one of the crucial
challenges in T2DM treatment [30]. The schematic diagram of the mechanism
of action of the phenolic acid in tea and coffee on diabetes are given in Figure
3. Additionally, green tea extract can prevent carbon tetrachloride (CCl4)
induced hepatic fibrosis and oxidative stress by increasing antioxidant enzyme
activities and inhibiting oxidative damage due to its phenolic acid content
[216]. Gallic acid also exhibited protective activity towards DNA and
membranes against ionizing radiation in both in-vitro and in-vivo studies.
Additionally, lipid peroxidation and cellular DNA damage reduction by gallic
acid in mice has been reported [217].
4.2.2. Anti-Cancer Properties

Science ancient times, tea has been used as a medicinal plant to treat
different diseases. In addition, anti-cancers properties of tea phenolic contents
are well established. Especially, the tea major phenolic acid, gallic acid
possesses chemopreventative effects against different types of cancer such as,
prostate, lung, breast, colorectal, esophageal, gastric, hepatic, lymphoma,
leukemia, osteosarcoma and melanoma cells [218-220]. Gallic acid derivatives
are marked free radical scavengers as well as inducers of differentiation and
apoptosis in leukemia, lung cancer, colon cancer cell lines, prostate cancer,
stomach cancer, cervical cancer, and normal lymphocyte cells. Additionally,
they can also prevent malignant transformation and cancer development [219,
221-228].
The anticancer activities of gallic acid and its derivatives include a number
of mechanisms such as, programmed cell death induction in malignant cells,
generation of ROS, regulation of apoptotic and non-apoptotic proteins,
suppression of oncogenes, inhibition of matrix metalloproteinase (MMPs),
activation of caspase-3, caspase-8, caspase-9, p53, c-Jun N-terminal kinases
(JNK) signaling pathways and cell cycle arrest in the G0/G1/M phase of the
cell cycle [218]. Gallic acid derivatives have also been found to inhibit
invasion and metastasis. Several green tea potential polyphenols including
(CA, gallic acid, catechin, epicatechin, gallocatechin, catechin gallate,
gallocatechin gallate, epicatechin gallate, epigallocatechin, epigallocatechin
gallate) have been investigated for their anticancer activity [220]. In this study,
the authors group found that the gallic acid significantly enhanced the
catechin’s anticancer properties. The structure activity relationship analysis
showed that after esterification of catechin units with gallic acid, the
antiproliferative activity significantly increased. Another report showed that,
when the epicatechin structure was modified from epicatechin gallate to gallic
acid it enhanced the antioxidant activity [229].
The antiproliferative activity of phenolic acids formed during human
intestinal microbial fermentation of green tea (GT) and black tea (BT) have
been reported [230]. The authors of the study demonstrated that, during the
fermentation of flavonoids from GT and BT by intestinal microbes in an in-
vitro model TIM-2, it produces a number of phenolic acids. Among these
phenolic acids 3, 4-dihydroxyphenylaceticacid exhibited the potential
antiproliferative activity against prostate and colon cancer cells. Black and
green tea extracts have inhibitory effects against tumor proteasome activity
[231]. This study also found that, black tea extract was more potent than green
tea due to its phenolic contents.
Gallic acids exhibited anticancer activity against two cancer cell lines,
human colon cancer cell line HCT 15 and the human breast cancer cell line
MDA MB 231 [226]. Results showed that the IC50 values of gallic acid were
96 µg mL-1 and 80 µg mL-1 against HCT 15 and MDA MB 231 cells
respectively. The anticancer properties of gallic acid against the A 549 human
lung adenocarcinoma cell line has been also reported [232]. Gallic acid exerted
a dose dependent inhibition of the A 549 cell line and induced apoptosis by
ROS (reactive oxygen species) elevation; MMP (mitochondrial membrane
potential) disruption and casepase-3 activation. As well as, HeLa cervical
cancer cells were inhibited by gallic acid through apoptosis [233].
4.2.3. Neuroprotective Activity

Tea phenolic acid dominates neuroprotective activity. Acrylamide is a
chemical compound which is associated with a number of harmful health
effects including neurotoxicity, reproductive toxicity, genotoxicity,
carcinogenicity, and mutagenicity. [234]. Basically, it is formed naturally in
foods those are rich in sugars and cooked at high temperatures. It has been
reported that green tea extracts and their major phenolic acid derivative, gallic
acid showed protective effects against acrylamide induced brain damage [235].
The genotoxic and neurotoxic effects of acrylamide were reduced with the
treatment of potential antioxidant gallic acid and green tea extract. Green tea
leaf (GTLs) extracts and their constituents such as gallic acid exerted activity
against kainic acid (KA) induced seizure in in-vitro studies [234]. Generally,
KA is a chemical compound that induces nerve excitability and causes neuron
epilepticus and excitotoxicity with the increased production of reactive oxygen
species (ROS) and lipid peroxidation [237-239]. The results showed that GTLs
and gallic acid exhibited reduced seizure patterns and lipid peroxidation.
Finally, the authors concluded that, the gallic acid from the fresh green tea
leaves was responsible for these neuroprotective activities. The
neuroprotective activity of gallic acid has also been reported by others [240-
244]. Gallic acid also exhibited neuroprotective activity against 6-
hydroxydopamine (6-OHDA) induced oxidative stress [244]. Oral
administration of gallic acid resulted in significant increase of passive
avoidance memory, total thiol, and glutathione peroxidase (GPx) contents and
decreased malondialdehyde (MDA) levels.
4.2.4. Antimicrobial Activity

Antimicrobial properties of tea phenolic acid have been demonstrated by
many studies [245-249]. Bioactive compound in tea, gallic acid has potential
antimicrobial properties [250-255]. Generally the level of inhibition depends
on the bacterial strain and the chemical structure of the compounds [249]. But,
the authors of this study, found no specific chemical structure activity
relationship for the inhibition of bacterial growth, neither methyl esterification
of gallic acid, para-hydroxyl group on the aromatic acid 3-phenylpropanoic
acid, nor the length of phenolic acid carbon chain. The authors group
investigated the effects of tea phenolic components and their aromatic
metabolites including catechin, epicatechin, 3-o-methyl gallic acid, gallic acid
and CA on bacterial growth. Fecal homogenates containing bacteria
significantly catalyzed these tea phenolic compounds to generate aromatic
metabolites. Different intestinal bacterial strains showed varying degrees of

growth sensitivity to tea phenolics and metabolites. The growth of pathogenic
bacterial strains such as Clostridium perfringens, Clostridium difficile, and
Bacteroides spp., was significantly inhibited by tea phenolics, whereas-,
commensal anaerobes and probiotics such as Clostridium spp, Bifidobacterium
spp, and Lactobacillus sp. were less affected. These results manifested that,
the tea phenolic acids possess positive effects on intestinal environment by
significantly modifying intestinal bacterial growth, presumably by acting as
metabolic prebiotics.
CA is commonly present in tea [256] and showed significant antibacterial
activity against E. coli, Pseudomonas, Clostridium and Bacteriodesm [249].
The effects of five commercial tea extracts (green, oolong, black, pu-erh and
chrysanthemum) and two tea components (EGCG and gallic acid) against oral
pathogens including S. mutans, S. S. mitis, S. salivaris, and Actinomyces
naeslundii have been demonstrated [257]. In this study tea extract was found
to inhibit bacterial strains by reducing the attachment of oral pathogens to
gingival tissue. Green tea and black tea extracts have antibacterial activity
against the carcinogenic bacterial strain S. mutans [258]. Both green and black
tea extracts significantly inhibit this bacterial growth. Specifically, ethyl
acetate and n-butanol extracts of green and black tea showed strong
antibacterial activity. Whereas, gallic acid content was higher in ethyl acetate
and n-butanol extracts of black tea leaves and esterified gallic acid was found
in the nondialyzable fraction of black tea. The antibacterial activity of gallic
acid was higher than that of catechin. Esterified gallic acid also showed
potential antibacterial activity. The synergistic and antagonistic effects of
green and black tea extracts with certain antibiotics against Streptococcus
pyrogenes have been determined [259]. The results showed that both tea
extracts completely inhibited the bacterial growth and found to have either
synergistic or antagonistic effects at different concentration on the selected
antibiotics. Among the different tea components, gallic acid induced the
antibacterial effects of all antibiotics in a dose dependent manner. The activity
was most prominent with black tea. The authors of this study suggested that
the antibacterial effects of gallic acid as nutritional supplements should be
subjected for future studies. Gallic acid exerted higher inhibitory activity
against H. pylori strains compared to catechin [260]. Gallic acid also showed
activity against E. cloi, P. aeruginosa, S. aureus, and L. monocytogens [261].
Here, gallic acid led to irreversible changes in membrane properties (charge,
physicochemical properties and intra and extra-cellular permeability) via
hydrophobicity changes, decreases of negative surface charge, and occurrence
of local rupture or pore formation in the cell membrane with consequent

leakage of essential intracellular components. Phenolic acids identified from
tea associated with health benefits are given in Table 4.
Table 4. Summary of the health benefits of tea phenolic acids
Tea Phenolic acid Heath benefits References

Green tea Gallic acid Anticancer [220]
Green and black tea 3,4-dihydroxyphenylaceticacid Anticancer [230]
Oolong tea Gallic acid Anticancer [212]
Black tea Gallic acid Antimicrobial [258]
Black tea Gallic acid Antimicrobial [259]
Tea Caffeic acid Antimicrobial [256]
Green tea Gallic acid Neuroprotective [235]
Green tea Gallic acid Neuroprotective [236]
CONCLUSION
Needless to say, tea and coffee are worldwide popular beverages and are
used as tremendous sources of phenolic acids. As underlined in our review,
phenolic acids in tea and coffee clearly possess humongous health benefits.
Phenolic acids like, hydroxybenzoic acids and hydroxycinnamic acids act as
potential agents for treating different health complications. Hydroxycinnamic
acids, particularly chlorogenic acid (CGA) derivatives from coffee can be used
as the vital source to treat diabetics, cancer, and cardiovascular disorder. Tea is
also associated with different beneficial effects which are related to the
presence of their phenolic acids. Further research should aim at isolating
phenolic acids from teas and then observe their health effects. To fully exploit
the beneficial effects of phenolic acids from tea and coffee, they should be
isolated from their target sources and their exact mechanism of action should
be studied for each specific disorder to further clarify how these versatile
compounds works.
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BIOGRAPHICAL SKETCH
Name: Jong-Bang Eun
Affiliation: Department of Food Science and Technology, Chonnam

National University
Education:
Postdoctoral Research, Food Science and Technology, 1991-1992.
Mississippi State University, Miss. State, MS
Ph.D., Food Science and Technology with Biochemistry Minor, 1987-
1991. Mississippi State University, Miss. State, MS
M.S., Food Science and Technology, 1983-1985. Chonnam National
University, Gwangju, KOREA
B.S., Food Science and Technology, 1977-1981. Chonnam National
University, Gwangju, KOREA
Business Address:
Chonnam National University
Food Science and Technology Program
Division of Food Technology, Biotechnology and Agrochemistry
77 Yongbong-ro Buk-gu
Gwangju, 61186, KOREA
TEL: +82-62-530-2145; FAX: +82-62-530-2149
Email: jbeun@jnu.ac.kr; jbeun@chonnam.ac.kr; jongbang@hotmail.com
Research and Professional Experience:

Appointments
2003. 10 - Present: Professor, Food Science and Technology Program,

Division of Food Technology, Biotechnology and Agrochemistry,
Chonnam National University, Korea.
2015. 1 – 2015. 12: Division Chairman, Division of Food Technology,

Biotechnology and Agrochemistry.
2012. 4 – 2015. 12: Organizing Committee. ICoFF 2015.
2011. 03 - 2015. 02: Director, Functional Food Research Center, Chonnam
National University, Korea.
2008. 8 - 2010. 8: Vice Dean, College of Agriculture and Life Sci., Chonnam
National University, Korea.
2004. 8 - 2005. 8: Visiting Professor, Division of Food System and Biological
Engineering, University of Missouri-Columbia, MO, USA.
2003. 8 - 2004. 8: Vice Dean, Long-Life Education Center, Chonnam National
University, Korea.
2000. 8 - 2002. 8: Department Chairman, Department of Food Science and
Technology, Chonnam National University, Korea.
2000. 6 - 2000. 8: Visiting Associate Professor, Virginia Seafood Agricultural
Research and Extension Center, Virginia Tech., Hampton, VA, USA.
1999. 12 - 2000. 2: Visiting Associate Professor, Virginia Seafood
Agricultural Research and Extension Center, Virginia Tech. Hampton,
VA, USA.
1999. 6 - 1999. 8: Visiting Scientist, Department of Food Science, Rutgers
University, New Brunswick, NJ, USA.
1998.10 - 2003. 10: Associate Professor, Department of Food Science and
1998. 6 - 1998. 8: Visiting Scientist, Horticultural Crops Quality Lab. USDA-
ARS, Beltsville, MD, USA.
1998. 1 - 1998. 2: Visiting Scientist, Department of Food Science and Human
Nutrition, University of Florida, USA.
1997. 6 - 1997. 8: Visiting Assistant Professor, Food Science and Engineering
Unit, University of Missouri-Columbia, MO, USA.
1996. 12 - 1997. 2: Visiting Scientist, Department of Food Science and
Technology, University of Georgia, GA, USA.
1993. 12 - 1994. 2: Visiting Assistant Professor, Department of Food Science
and Technology, Mississippi State University, MS, USA.
1993. 6 - 1993. 8: Visiting Assistant Professor, Department of Food Science
1992 - 1998: Assistant Professor, Department of Food Science and
1991 - 1992: Post-Doctoral Research Associate, Department of Food Science
1988 - 1991: Graduate Research Assistant, Department of Food Science and

Technology, Mississippi State University, MS, USA.
1986 - 1987: Instructor, Department of Food Science and Technology,
Chonnam National University, Korea.
1984 - 1985: Graduate Research Assistant, Department of Food Science and
1983 - 1984: Graduate Teaching Assistant, Department of Food Science and
Professional Activities
- Editorial Board
Sky J. Food Sci. Technol.

Editor-in-Chief, 2013. 1 - Present
Safe Food
Editor-in-Chief, 2013. 1 - 2014. 12
Food Science and Technology Letters

Associate Editor, 2013.1 - 2016. 01
J. Food Agric. Environ.

Editorial Board, 2000 - 2005
Am. J. Food Technol.

Editorial Board, 2006 - 2008
Food Sci Biotechnol.

Editor, 2004 - 2006; Editorial Board, 2007 - 2011
J. Korean Soc. Food Sci. Nutr.

Editor-in-Chief, 2008. 1 - 2008. 12
J. Food Preservation
Editorial Board, 1995 - Present
J. Korean Tea Society

Editorial Board, 2000 - Present; Editor-in-Chief, 1997 - 2000
Am. J. Adv. Food Sci. Technol.

Editorial Board 2013. 5 - Present
- Professional Society
Korea Taste & Food Center

Board Executive Officer, 2012 - Present
The Korean Society of Food Preservation

Treasurer, 1993 - 1995; President, Honnam Regional Section, 1999 -
2001; Secretary of Scientific Affair, 2002 - 2004; Secretary of General Affair,
2004 - 2006; President of Jeolla-Jeju Regional Section, 2006 - 2008; Secretary
General, 2009. 1- 2009. 12; Audit, 2010 - 2011; Vice President, 2013. 1-
2014.12
Naju Natural Colorants Industrial Support Center

Consulting Committee, 2012-2014
Korean Food & Drug Administration

National Food Safety Committee 2005-2007; National Functional Food
Committee 2007-2009; Professor Support Committee, 2011-Present
Korean Society of Food Science and Technology

Managing Editor, 2001.1 - 2001.12; Secretary, Honam Regional Section,
1995-1997, 2001-2002; Editorial Board, 1998 - 2002; Secretary of Special
Affair, 2003. 1 - 2003. 12; Fellow, 2002 - Present; Chairman of Seafood
Division, 2004. 6 - 2006. 6; Secretary of Scientific Affair, 2006. 1 - 2006. 12;
Vice President, Honam Regional Section, 2008. 1 - 2008. 12; President,
Honam Regional Section, 2011. 1 - 2011. 12; Secretary of General Affair,
2012.1 - 2012. 12; Secretary General 2015.1 - 2015.12
Korean Society of Food Science and Nutrition

Editorial Board, 1999-2002; Secretary of Scientific Affair, 2002.1-
2002.12; Secretary of General Affair, 2002.1 - 2002.12; Audit 2009. 1 -
2009.12; President of Jeolla-Jeju Regional Section, 2010. 1- 2010. 12
Korean Society of Food Preservation,

Editorial Board, 2005-Presnet; Secretary of Scientific Affair, 2007.1-

2007.12; Secretary of General Affair, 2009.1 -2009. 12; Audit 2010. 1 -
2010.12; President of Jeolla-Jeju Regional Section, 2008. 1- 2008. 12
Vice President, 2011 1 -2013. 12
International Society of Horticultural Science

Member, 1997-2001
American Chemical Society

AGFC Division Member, 1996-Present
The Korean Tea Society

Secretary, 1994 - 1997; Executive Fellow, 2000 - 2007; Secretary of
General Affair, 2006. 1 - 2006. 12; Vice President, 2008. 1- 2013. 12; 2014. 1
– 2015. 12, President
The Korean Fisheries Society

Member, 1992 – 2010; Fellow, 2011- Present
Institute of Food Technologists

Student Member 1987-1992; Seafood Division & Int’l Division Member,
1978-Present; Professional Member, 1992 - Present; Subpanel of Food
Packaging and Processing, 2011. 6 - 2012.6; 2014 TRP Abstract Reviewer,
2013 - 2104; 2015 Annual Meeting Scientific Program Track Team Reviewer:
Food Processing & Packaging Track, 2014-2015; IFT16 Track Team
Reviewer, 2015-2016
The Phi Tau Sigma Honorary Society

Member, 1988-1992
Refereed publications:
Gui-Hun Jiang, Seung-Hee Nam, Sun-Hee Yim, Young-Min Kim, Hyun Jung
Gwak, and Jong-Bang Eun. 2016. Changes in Total Phenolic and
Flavonoid Content and Antioxidative Activities during Production of
Juice.
Concentrate from Asian Pears (Pyrus pyrifolia Nakai). Food Sci. Biotechnol.
25(S): 47-51.
Seung-Hee Nam, Young-Min Kim, Marie K. Walsh, Sun-Hee Yim, and Jong-
Bang Eun. 2016. Functional Characterization of Purified Pear Protease
and Its Proteolytic Activities with Casein and Myofibrillar Proteins. Food
Sci. Biotechnol. 25(S): 1-9.
Quang-Vinh Nguyen, Van Bon Nguyen, Jong-Bang Eun, San-Lang Wang,
Dinh, Hoang Nguyen, Thi Nhung Tran & Anh, Dzung Nguyen. 2016.
Anti-oxidant and antidiabetic effect of some medicinal plants belong to
Terminalia species collected in Dak Lak Province, Vietnam. Res Chem
Interm. 42:5859-5871.
Quang-Vinh Nguyen, Kim Duwoon, San-Lang Wang, Jong-Bang Eun. 2016
Effect of Terminalia nigrovenulosa extracts and their isolated compounds
on intracellular ROS generation and MMP expression in HT1080 cells.
Res Chem Intermed. 42:2055–2073.
Hyeon-Jin Park, Yongjae Lee, Jong-Bang Eun, 2016. Physicochemical
characteristics of kimchi powder manufactured by hot air drying and
freeze drying. Biocatalysis & Agric. Biotechnol. 5:193-198.
Anggi Hayu Hapsari, Seon-Jae Kim, Jong-Bang Eun, 2016. Physical
characteristics of parboiled Korean glutinous rice (Olbyeossal) using a
modified method, LWT-Food Sci Technol. 68:499-505.
Anggi Hayu Hapsar,and Jong-Bang Eun, 2016. Microstructure of Olbyeossal,
Partially Milled Parboiled Glutinous Rice Made by Modified Parboiling
Method, Food Sci. Biotechnol. 25(2)1-5.
Gui-Hun Jiang, Young-Min Kim, Seung-Hee Nam, Sun-Hee Yim, and Jong-
Bang Eun, 2016. Enzymatic Browning Inhibition and Antioxidant Activity
of Pear Juice from a New Cultivar of Asian Pear (Pyrus pyrifolia Nakai
cv. Sinhwa) with Different Concentrations of Ascorbic Acid, Food Sci.
Biotechnol. 25(1): 153-158.
Ji-Hyun Min and Jong-Bang Eun. 2016. Physicochemical and Sensory
Characteristics of Persimmon Jelly Added with Different Levels of
Daebong Persimmon Puree. Kor. J. Food Sci. Technol. 48(1):54-58.
Pyo-Hyeon Kim, In-Sook Kim, Jong-Bang Eun. 2015. Functions of green tea
extracts used in food. 21(2) 101-105.
Nguyen, Q.V., Nguyen, N.H. and Eun, J.B. 2015. Antioxidant activity of
Terminalia nigrovenulosa and Premna integrifolia extracts in soybean oil.
International Food Research Journal 22(1): 254-261.
Hyun-Jung Kim, Yong Jae Lee, Jong-Bang Eun.2015. Effects of ultraviolet
radiation on the physicochemical characteristics of Korean native cattle
(Hanwoo) beef. J Korean Soc Appl Biol Chem 58(1)149-156.
Yu-Rim Shin, Ki-Chang Lee, Jong-Bang Eun. 2015. Physicochemical

Characteristics and Sensory Evaluation of a Green Tea Infusion Extracted
with Different Amounts at Room Temperature (25℃). J. Korean Tea Soc.
21(1) 46-52.
Hyun-Jung Kim, Yong-jae Lee, Jong-Bang Eun. 2014. Changes in the
Microbiological Characteristics of Korean Native Cattle (Hanwoo) Beef
Exposed to Ultraviolet (UV) Irradiation Prior to Refrigeration. Korean J.
Food Sci. An. 34(6) 815-821.
Jong-Bang Eun, Mi-Yeon Jo, Ji Soon Im. 2014. Physicochemical
characteristics of coffee extract using different extraction methods. J.
Korean Food Sci. & Technol. 46(6) 723-728.
Seo-Woo Beom, Gui-Hun Jiang and Jong-Bang Eun. 2014. Effect of
blanching time on physicochemical characteristics and sensory evaluation
of Aster scaber. Korean J. Food Preserv. 22(1) 51-55.
Yong-Chan Seo, In-Sook Kim, Dong-Ok Chung, Jong-Bang Eun. 2014.
Physicochemical properties and sensory evaluation of a green tea infusion
extracted from green tea for cold water extraction at low temperatures (5
and 25℃) for different times. J. Korean Tea Soc. 20(4) 91-97.
Nam-Sook Kim and Jong-Bang Eun. 2014. Tea culture therapy program for
adaption of multicultural families. J. Korean Tea Soc. 20(3) 14-19.
Jong-Bang Eun, Fu-hung Hsieh and Ok-Ja Choi. 2014. Physicochemical
properties of rice-based expanded snacks according to extrusion
conditions. J. Korean Soc. Food Sci. Nutr. 43(9) 1407-1444.
Awards:
Korea President Award 5. 14. 2015, Korean Government

Distinguished Lifetime Achievement Award in Kor. Soc. Food Preserv. 6.
14, 2014. Kor.Soc. Food Preserv.
Award for Excellent Paper in Science and Technology, 7. 5. 2011, Kor.
Found. Sci. Technol.
Award for Excellent Paper in Science and Technology, 7. 5. 2008, Kor.
Found. Sci. Technol.
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Phenolic acids in tea and coffee and their health beneﬁts

Chapter · January 2016

Protiva Rani Das Jong-Bang Eun

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PHENOLIC ACIDS IN TEA AND COFFEE

Protiva Rani Das1,2 and Jong-Bang Eun1

strong antioxidants that possess anti-carcinogenic, antitumor,

Keywords: phenolic acid, tea, coffee, health benefits

2. GENERAL ASPECTS OF TEA AND COFFEE

Interestingly, next to water, tea is the most consumed beverage in the

reasons are responsible for worldwide popularity of coffee, including its

3. IDENTIFIED PHENOLIC ACIDS IN TEA AND COFFEE

It is well known that the major polyphenols in C. sinensis are a number of

Figure1. Structures of identified phenolic acid derivatives in tea.

Table1. Phenolic acid derivatives in tea

Phenolic acid Sources References

3.2. Phenolic Acids in Coffee

Among various types of beverages coffee is the affluent sources of

conjugated structures. Furthermore, the major CGA conjugates in coffee have

3-0-caffeoylquinic acid 4-0-caffeoylquinic acid

5-0-caffeoylquinic acid 3-0-feruoylquinic acid

4-0-feruoylquinic acid 5-0-feruoylquinic acid

3-0-dimethoxycinnammoylquinic acid 4-0-dimethoxycinnammoylquinic acid

5-0-dimethoxycinnammoylquinic acid 3,4-di-0-caffeoylquinic acid 3,5-di-0-caffeoylquinic acid

4,5-di-0-caffeoylquinic acid 3,4-di-0-feruloylquinic acid 3,5-di-0-feruloylquinic acid

4,5-di-0-feruloylquinic acid 3-0-feruoyl, 4-0-caffeoylquinic acid 3-0-caffeoyl, 4-0-feruloylquinic acid

3-0-feruloyl, 4-0-dimethoxycinnammoylquinic acid 3-0-dimethoxycinnammoyl, 5-0-feruloylquinic acid

3-0-feruloyl, 5-0-dimethoxycinnammoylquinic acid 4-0-dimethoxycinnammoyl, 5-0-feruloylquinic acid

4-0-feruloyl, 4-0-dimethoxycinnammoylquinic acid 3-0-caffeoylquinic acid lactone

4-0-caffeoylquinic acid lactone 4-0-p-coumayolquinic acid

5-0-p-coumayolquinic acid Caffeic acid

Ferulic acid 1-0-dimethoxycinnamoylquinic acid

Figure 2. Structures of identified phenolic acid derivatives in coffee.

Table2. Phenolic acid derivatives in coffee’

Phenolic acid Sources References

Phenolic acid Sources References

4. HEALTH SIGNIFICANCE OF PHENOLIC ACID

4.1.1. Antidiabetic Activity

4.1.1.1. α-glucosidase and α-amylase Inhibition

4.1.1.2. AMPK Activation

4.1.1.3. Inhibit the Expression of G-6-Pase

The antidiabetic effect of ferulic acid (FA) was demonstrated by a number

4.1.2. Cardiovascular Activity

4.1.3. Anticancer Properties

and prevent 4-nitroquinolone 1-oxidase –induced oral carcinogenesis in rats

inflammatory interleukin 6 (IL6). The authors group concluded that, MB

carcinogenesis. Coffee extracts from C. arabica and C. robusta showed

Table 3. Summary of the health benefits of coffee phenolic acids

Coffee Phenolic acid Heath benefits References

C. Arabica & CGA, CA Antimicrobial [190]

Coffee Phenolic acid Heath benefits References

4.2. Health Benefits of Tea Phenolic Acids

4.2.1. Anti-Diabetic Activity

significantly induced diuresis in a dose dependent manner. The study also

Figure 3. Overview of the mechanisms of action of phenolic acids of coffee and

The antidiabetic mechanism of gallic acid has been described in detail

4.2.2. Anti-Cancer Properties

4.2.3. Neuroprotective Activity