BIOCHEMISTRY OF

DIGESTIVE SYSTEM
 
1,2
Marhaen Hardjo
1
Head of Biochemistry Department, Medical Faculty of Hasanuddin University
2
Director of Stem Cell Center Hasanuddin University Hospital
 

DEPARTMENT OF
BIOCHEMISTRY MEDICAL
FACULTI OF HASANUDDIN
UNIVERSITY
Digestion
 Digestion – The process of changing food
into simple components which the body can
absorb

 Digestive tract or Gastrointestinal tract-

where digestion & absorption take place

 Mouth->esophagus->stomach->small
intestine->large intestine
GI Tract Anatomy
 Digestion
 Mouth – ingestion of food; chewing
(mastication) & swallowing
1. Bolus – portion of food swallowed
at one time
2. Saliva - water, salts, enzymes,
mucus secreted by salivary glands
to:
a. Moisten food & aids swallowing
b. Begins carbohydrate digestion
Secretions of Digestion
I. Salivary secretion

6
Salivary gland

7
 Secretion
Saliva: water, ions, mucus, enzymes

Acinar Cells: 腺
泡细胞

8
Functions of secretion

1. Moisten food
2. Begin chemical digestion (a amylase, 淀
粉酶 )
3. Adjust appetite
4. Bacteriostatic action （抑菌作用 )
(bacteriolysin, 溶菌素 ) 9
Control of salivary secretion
Fear Nausea
Sleep
Secretion rate depends Tired
Dehydration

entirely on neural control

both parasympathetic (Ach,
M receptor) (water
secretion)
and sympathetic (NA, β
receptor) (enzyme) SNS (cAMP) PNS(IP3)

lead to increased secretion Secretion

Vasodilation
Cell contraction
Metabolism 10
SALIVA
MALTOSA
KANJI (STARCH) AMILASE LIUR MULUT +
NASI, ROTI (PTYALIN) MALTOTRIOSA
GLIKOGEN +
DEXTRIN
Amilase liur mulut :
 Menghidrolisis ikatan 1-4 Glikosida
 Tidak aktif pada Ph<4
Enzim-enzim Lambung :
Pepsin
 Dihasilkan oleh “Chief Cell” dalam bentuk Zimogen in-
aktif (Pepsinogen)
 Pepsinogen oleh H+ menjadi Pepsin
 Suatu Endopeptidase
Memecah ikatan peptida pada Struktur Polipeptida Utama
SALIVA

Renin (Khimosin, Rennet) Koagulasi susu pada infan

Renin Pepsin
Kasein Susu Para Kasein
Digestion
 Esophagus – connects mouth to stomach
1. Epiglottis – closes airway

2. Bolus moved along by peristalsis

3. Cardiac sphincter – keeps food from

backing up into esophagus
Digestion
 Stomach – collecting & churning
1. Gastric glands secrete: gastric juice
(water, enzymes, hydrochloric acid) that
kills most bacteria and begins protein
digestion and mucus to protect lining
2. Chyme – semi-liquid mass of partially
digested food
3. Pyloric sphincter – regulates passage
of chyme into small intestine
Secretions of Digestion
II. Gastric secretion

16
 Functions of Stomach
• Temporary store of ingested material
• Dissolve food particles and initiate
digestive process
• Control delivery of contents to small
intestine
• Sterilise ingested material
• Produce intrinsic factor (Vitamin B12
absorption)
17
 Oesophagus
Lower Oesophageal
Sphincter
Fundus

Duodenum
Pylorus

Body

18
Antrum
Functional Anatomy of Stomach
Oesophagus

Fundus Lower Oesophageal

Sphincter
Fundus

• Storage
Body
• Storage Duodenum

• Mucus Pylorus

• HCl Body

• Pepsinogen Antrum

• Intrinsic factor
Antrum
• Mixing/Grinding
• Gastrin
19
 II.1 Gastric gland cells
1. Oxyntic gland ( 泌酸腺
）
Parietal cell
Chief cell
Mucous neck cell
2. Pyloric gland
Mucus cell
3. Cardiac gland
Mucus cell
4. Endocrine cells (G, D, ECL)
ECL:enterochromaffin-like cell
20
Exocrine gland cells of gastric pits

Produce alkaline
mucus that covers
mucosa layer

Synthesize and
secrete the protease
precursor known as
pepsinogen.

Synthesize and
secrete the HCl acid
responsible for the
acidic pH in the
gastric lumen.

21
Structure of Stomach Wall

22
 II.2 Composition and function of
gastric secretions
1. HCl
 converts pepsinogen to pepsin for chemical
digestion
 provides optimal pH environment for pepsin
 destroys some bacteria
 stimulates the small intestinal mucosa to release
secretinand CCK
 promotes the absorption of Ca2+ and Fe2+ in small
intestine 23
 Composition and function of
gastric secretions

2. Pepsinogen (precursor of pepsin)

 digestion of proteins

3. Mucus
 forms a protective barrier: Mucus-bicarbonate
barrier
4. Intrinsic factor
 combines with vitamin B12 to make it absorbable

24
HCl secretion

光面管泡

微管

25
HCl secretion

26
HCl secretion

27
 K
H2O Stomach
Lumen
pH<2

~
Cl H Carbonic
Anhydrase

H2CO3 CO2 + H2O

HCO3

pH>7.4
CO2
28
Cl Blood
 Inactive precursor of pepsin
which initiates protein digestion
Cells Is not necessary for complete
digestion of dietray protein –
pancretic enzymes are sufficient
Active only when the pH < 3.5

29
Physical/chemical barrier
to attack by gastric juice
Stimulated by:
• Ach
• Mechanical Stim
• Chemicals (ethanol)
If breached e.g.
hypersecretion of acid -
ulceration 30
Gastric Mucus-Bicarbonate Barrier

31
 Gastric Mucus-bicarbonate barrier

The insoluble mucus and bicarbonate

construct a barrier
prevent hydrogen ions from diffusing to
the mucosal layer
protect the stomach mucosa from injury
by hydrochloric acid and pepsin,

32
Intrinsic Factor
Only gastric secretion that is Essential for health
Secreted from parietal cells in humans, chif cells in
other species
Forms a complex with vitamin B12 in the gut
The complex is resistant to digestion and therefore
enables absorption of vitamin B12
Lack of intrinsic factor causes Vit B 12 deficiency
(pernicious anaemia) – as all the Vit B 12 is digested
and therefore can not be absorbed 33
II.3 Regulation of
Secretion

34
 Control of Gastric Acid Secretion

Gastric acid secretion is controlled by three

mechanisms:

 Neurocrine (vagus/local reflexes)

 Endocrine (gastrin)
 Paracrine (histamine)

35
Endocrine gland cells of gastric pits

Stimulates acid
secretion

Inhibits
• acid secretion
• gastrin and pepsin
release
• pancreatic exocrine
secretions

Stimulates acid
secretion
36
 Regulation of Gastric Secretions
The important stimulatory signals
Autonomic nerves
• Release ACh
• Stimulates smooth muscle contraction
• Also stimulates Chief , Parietal , ELC and G cells
Gastrin
• Stimulates Chief , Parietal , ELC cells
Histamin
• Stimulates Parietal cells
Protein products such as peptides, A.A’s
• Stimulates G-cells
Acids 37

• Stimulate D cells
 Endogenous substances regulating
gastric secretion

协同作用

38
GASTRIN
ACETYLCHOLINE
HISTAMINE

GS AC

Ca Ca
ATP cAMP

PROTEIN
KINASES

K
~ 39
 Gastric secretion
during digesting food

40
 Mechanisms Stimulating Gastric Acid
Secretion in Cephasic Phase
Cephalic Phase
Sight, smell, Vagus + Parietal
taste of food nerve ACh cells

GRP
G cells
+ +
Gastrin

ECL Histamine
Gastrin/ACh
cells
41
 Cephalic Phase
1. Cephalic phase

 Occurs before food enters the stomach;

 initiated by smell, taste, sight Impulses from
olfactory, chemical and other receptors activate the
vagal nuclei in the medulla (via Hypothalamus)
 This triggers motor impulses to travel via the
vagus nerve to the parasympathetic enteric ganglia
 Enteric ganglia in turn stimulate stomach glands

42
Cephalic Phase
Unconditioned and conditioned reflex
Only occurs when we want food
depression dampens this reflex
Account for 10% - 15% total volume of secretion
Large amount of HL and pepsinogen, high digestive
ability

43
 Gastric Phase
Distension Vagal/
of stomach Enteric
(arrival of food) reflexes ACh

Peptides Gastrin Parietal

G cells
in lumen cells

ECL Histamine
Gastrin/ACh
cells
44
 Starts when food reaches the stomach
 Provides 2/3 of the juice released
 There are two parts (neural and chemical) to this phase
• Neural part
 Activated by stretch receptors
 Initiates both local neural reflexes as well as the longer
vago-vagal reflex
 Both reflexes result in release of ACh at stomach synapses
which stimulates secretory cells
 This branch is inhibited by Sympathetic action (emotional
upset) 45
Chemical part

An increase in pH (thus, ‘less’ acidity), presence of peptides,

caffeine activate the G-cells

This results in Gastrin being released

Gastrin acts on Parietal cells that start secreting HCl

Gastrin also stimulates Histamine release, which in turn

stimulates Parietal cells

The increase in HCl promotes pepsin production and protein

degradation
46
Chemical part

The release of Gastrin is partly regulated by acidity

Increased acidity inhibits the G-cells
Increased presence of proteins in a meal tends to buffer
proton
This in turn keeps the pH from becoming too acidic
and allows more gastrin to be released

47
Intestinal Phase
Account for about 5% of secretion
Primarily hormonal – denervated stomach will
be stimulated to secrete acid by protein in
duodenum
Hormone still unknown
Very smalll number of G-cells in duodenum
also release gastrin in response to amino acids
48
Regulation of Gastric Secretions occurs via 3 phases

49
Mechanisms Inhibiting Gastric Acid Secretion
Cephalic Phase
Stopping eating Vagal activity
Gastric Phase
pH ( [HCl]) Gastrin
Intestinal Phase
Acid in Enterogastric Gastrin secrn
duodenum (splanchnic) reflex
Gastrin stimn
Secretin release of parietal
cells
Fat in GIP release Gastrin secrn
duodenum Parietal HCl secrn
50
 Enterogastrones
• Hormones released from gland cells in duodenal
mucosa - secretin, cholecystokinin (CCK), GIP
• Released in response to acid, hypertonic
solutions, fatty acids or monoglycerides in
duodenum
• Act collectively to prevent further acid build up
in duodenum
• Two strategies:
• inhibit gastric acid secretion
• reduce gastric emptying (inhibit
motility/contract pyloric sphincter) 51
 Regulation of gastric secretion

Mechanical
Hyperosmotic solution
stimulation
Entero-oxyntin
Fatty acids

HCl

Secretion of Ach or other transmitters

by nerve endings

Gastric gland

52
Gambar 1. Bagian dari lambung dan duodenum
 Pembentukan HCl lambung

Sumber H + adalah hasil pemecahan H2CO3 oleh

karbonik anhidrase.
H2CO3 ini dibentuk dari H2O dan CO2. Sekresi H+
kedalam lumen merupakan proses aktif melalui
membran dengan bantuan K+/ATP ASE.
HCO3 mengalir dari dalam sel Oksintik ke
plasma sebagai pengganti ion Cl yang
memasuki sel dari plasma sekresi H + ke dalam
Lumen. Sekresi H+ kedalam lumen diganti oleh
K+ kedalam Sel
 ( SEL OKSINTIK ) Cairan
Plasma Lambung
(Lumen)
CL
CL CL -P

K+ K+ K+
H+
-P
HCO3- HCO3 + H+

H2CO3

CO2 CO2 + H2O

Karbonik anhidrase
H2O H2O H2O
Gambar 1.2. sumber H+adalah hasil pemecahan
H2CO3 oleh karbonik anhidrase. H2CO3 ini dibentuk
dari H2O dan CO2. Sekresi H+ ke dalam lumen
merupakan proses aktif melalui membran dengan
bantuan K+/ATP ASE. HCO3 mengalir dari dalam sel
oksintik ke plasma sebagai pengganti ion Cl- yang
memasuki sel dari plasma akibat sekresi H+
kedalam lumen diganti oleh K+ ke dalam sel.
Faktor-faktor yang mempengaruhi
sekresi getah lambung

1. FASE SEFALIK : RANGSANGAN DARI DALAM KEPALA,

BAU, MENGUNYAH DAN MENELAN MAKANAN

2. FASE GASTER : PEREGANGAN LAMBUNG MERANGSANG

MELALUI N. VAGUS (N X) DAN REFLEKS LOKAL

3. FASE INTENSINAL : KHIME PADA BAGIAN PROKSIMAL

USUS MELAMBATKAN SEKRESI ASAM LAMBUNG
gambar 1.3. hubungan antara jumlah asam yang
disekresikan oleh lambung selama pencernaan
makanan dan kandungan protein makanan tersebut.
Jumlah asam disekresikan ditetapkan 100,
berdasarkan respons terhadap 100 kalori
daging sapi, kemudian dihubungkan dengan
kandungan protein daging sapi tersebut. Jumlah
asam yang disekresikan akibat pemberian makanan
(100 kalori) dihubungkan dengan kandungan
protein makanan tersebut. (sumber: Davenport
1984)
 FAKTOR-FAKTOR KETAHANAN MUKOSA LAMBUNG

1. MUKUS DAN BIKARBONAT

2. RESISTENSI MUKOSA : DAYA REGENERASI SEL

POTENSIAL LESTRIK MEMBRAN MUKOSA DAN
KEMAMPUAN PENYEMBUHAN LUKA

3. ALIRAN DARAH MUKOSA ( MIKRO SIRKULASI )

4. PROSTAGLANDIN
Gambar 1.4. Patofisiologi akibat terjadinya difusi balik asam melalui
barrier mukosa lambung yang rusak.
Digestion
 Small Intestine – 3 segments:
1. Duodenum – opening from common bile duct
secretes fluids from:
a. Liver & Gallbladder – bile emulsifies fat
b. Pancreas – amylase break down
carbohydrate, sodium bicarbonate
neutralizes the acidic chyme and lipase
2. Jejunum
3. Ileum
a. Ileocecal valve – sphincter that regulates
passage of chyme into large intestine
Digestion
 Large intestine (colon) - reabsorbing &
eliminating
1. Fermentation of undigested
residues by bacteria occurs
2. Terminates at rectum, where water
some minerals are absorbed
3. Anus – sphincter that controls
defecation (excretion of fiber
residue, wastes and some water)
The Final Stage
Digestion
 Muscular action helps to propel liquefied food
through the G.I. tract by:
1. Peristalsis – muscular contractions
that push contents forward
2. Segmentation – inward squeezing for
greater mixing of secretions
3. Sphincter contractions
Peristalsis
Segmentation
Sphincter Contractions
Digestion and Absorption

 Carbohydrates, proteins and lipids are

digested and absorbed in the small intestine
 Absorption
 The surface area for absorption in the small intestine is
greatly increased by the presence of the brush border
 Pathways of Absorption
- cellular
- paracellular
Structure of intestinal wall
 Longitudinal folds (finger-like villi)
- longest in duodenum & shortest in ileum
- increases surface area 600 fold
 The significance of villi & microvilli
- increase the surface area
- maximizing the exposure of nutrients to
digestive enzymes
III. Secretion of the pancreas

71
 Secretion of the pancreas
Endocrine - insulin & glucagon
Exocrine - enzymes and bicarbonate
essential for digestion
almost under separate hormonal control

72
 Gall bladder

Sphincter of Oddi 73
Anatomy and secretion

74
 Islet of Langerhans
(secrete insulin)

Acinus

Capillary

Acinar cells
(secrete enzymes)

Intercalated duct

Duct cells
(secrete HCO3)
To pancreatic duct
75
 Exocrine Pancreas
Responsible for digestive function of pancreas

•Anatomical Structure
Acini Ducts Pancreatic Duct

•Function
Secretion of bicarbonate by duct cells
Secretion of digestive enzymes by acinar cells

76
 Zymogens
• Acinar cells contain digestive enzymes stored as
inactive zymogen granules
• Prevents autodigestion of pancreas
• Enterokinase (bound to brush border of duodenal
enterocytes) converts trypsinogen to trypsin
• Trypsin converts all other zymogens to active
forms

77
Duodenum
 Categories of Pancreatic Enzymes

Proteases Cleave peptide bonds

Nucleases Hydrolyze DNA/RNA

Elastases Collagen digestion

Phospholipases Phospholipids to fatty acids

Lipases Triglycerides to fatty acids+

glycerol

Amylase Starch to maltose + glucose

78
 Activation of pancreatic proteases

Enterokinase
Trypsinogen Trypsin

Trypsinogen Trypsin
Chymotrypsinogen Chymotrypsin
Proelastase Elastase
Procarboxypeptidase Carboxypeptidase

79
 Bicarbonate secretion
Lumen Blood
H2O CO2 CO2
H2CO3
HCO3- HCO3-
H + H+

Cl- ATP
Cl -

Na+ Na+ Na+

H2O H2O
80
 Bicarbonate function

Function
1. Neutralize gastric
acid emptied into the
duodenum
2. Provide a favorable
alkaline environment
for optimal activity of
pancreatic enzymes
81
 Control of Pancreatic Function

• Bicarbonate secretion stimulated by secretin

• Secretin released in response to acid in
duodenum

• Zymogen secretion stimulated by

cholecystokinin (CCK)
• CCK released in response to fat/amino acids in
duodenum
• Also under neural control (vagal/local reflexes)
- triggered by arrival of organic nutrients in
duodenum 82
 Control of pancreatic secretion
- secretion in 3 phases
Cephalic phase - only 10-15% of total secretion
Activation of vagal efferent stimulates enzyme release

Gastric phase - only present in some species

NOT SIGNIFICANT IN HUMANS
Intestinal phase - majority of secretion
Combination of hormones CCK and secretin and
neuronal reflex
Results in maximal enzyme and bicarbonate 83
 Control of pancreatic secretion

Key hormones in stimulation of secretion

are:
Cholecystokinin (CCK) and Secretin
( released from the small intestine)
Inhibiting factors: SS, PP, glucagon

84
 Cholecystokinin
stomach
duodenum

CCK
I cells

Vagus afferent Peptides Amino CCK release peptide

acids, Fatty Acid H+
nerve – vagovagal
reflex
Fat pancreas

5-HT

Enzymes

85
 Secretin

H+
Fat
Peptides

S cells
HCO3-

Secretin
86
Control of Pancreatic Function

87
Intestinal phase of secretion
VAGUS

CCK
Peptides
Amino acids
Fat, H+

Secretin HCO3- ACh

Enzymes
88
GETAH USUS

ENZIM-ENZIM GETAH USUS

1. AMINOPEPTIDASE
EKSOPEPTIDASE : MENGHIDROLISIS IKATAN PEPTIDA
DISEBELAH ASAM AMINO TERMINAL DIPEPTIDASE
2. DISAKHARIDASE
MALTASE (∝- GLUKOSIDASE):
MEMISAHKAN GLUKOSA DARI 1-4 OLIGO-SAKHARIDA
ISOMALTASE (∝-DEKSTRINASE):
MENGHIDROLISA IKATAN 1-6 ∝- LIMIT DEKTIRIN
LAKTASE (β – GALAKTOSIDASE) :
MEMISAHKAN GALAKTOSA DARI LAKTOSA

SUKRASE:
MENGHIDROLISIS SUKROSA
ENZIM-ENZIM GETAH USUS
3. FOSFATASE
MEMISAHKAN FOSFAT DARI FOSFAT ORGANIK
4. POLINUKLEOTIDASE
MEMECAH ASAM NUKLEAT MENJADI NUKLEOTIDA
5. NUKLEOSIDASE (NUKLEOSIDA FOSFORILASE)
MEMECAH NUKLEOSIDA MENJADI BASA NITROGEN DAN
PENTOSA FOSFAT.
6. FOSFOLIPASE
MEMECAH FOSFOLIPID MENJADI GLISEROL, ASAM LEMAK,
FOSFAT DAN BASA KHOLIN.
 ENZIM-ENZIM PANKREAS
PROTEOLITIK :
TRIPSIN :
MEMECAH PEPTIDA PADA GUGUS ASAM AMINO BASA
KHIMOTRIPSIN :
MEMECAH IKATAN PEPTIDA PADA ASAM AMINO TIDAK BERMUATAN
(seperti ASAM AMINO AROMATIK)
ELASTASE :
MEMECAH IKATAN ASAM AMINO GLISIN, ALANIN DAN SERIN

ENTEROKINASE
TRIPSINOGEN TRIPSIN

TRIPSIN
KHIMOTRISINOGEN KHIMOTRIPSIN
ENZIM-ENZIM PANKREAS
KARBOKSIPEPTIDASE
EKSOPEPTIDASE : MEMECAH IKATAN TERMINAL KARBOKSI PEPTIDA
SEHINGGA MEMBEBASKAN ASAM AMINO TUNGGAL

AMILOLITIK ENZIM
∝-Amilase : Memecah Ikatan 1,4 Glikosida

LIPOLITIK ENZIM
Triggliserida Lipase Monogliserida
(Triasil Gliserol) + Asam Lemak

KOLESTRO ESTERASE
Ribonuklease dan Deoksiribonuklease
gambar 1.5. sekresi sel sentro asinar dan duktus
ekstralobularis pankreas. kadar Cl- pada bagian
kanan dihitung berdasarkan cairan yang
dikumpulkan dengan “macropunctur”, sedangkan
bikarbonat dihitung berdasarkan isotonik. Data-data
berasal dari pankreas kucing,
tetapi pada spsies lain juga secara bersamaan.
(sumber : Lightwood dan Robert, 1977)
 FOSFOLIPASE A1

H2C O C R1
O
FOSFOLIPASE D
R1 C O C H O

H2C O P O BASA NITROGEN

FOSFOLIPASE A2 O

FOSFOLIPASE C

Gambar 1.6. Tempat aktifitas hidrolisis oleh fosfolipase pada substrat fosfolipid.
(sumber; Mayes P.A., 1988)
Biochemistry of the liver
The figure was adopted from http://faculty.washington.edu/kepeter/119/images/liver_lobule_figure.jpg (April 2007)
The figure was adopted from http://connection.lww.com/Products/porth7e/documents/Ch40/jpg/40_003.jpg (April 2007)
The figure is from: Color Atlas of Biochemistry / J. Koolman, K.H.Röhm. Thieme 1996. ISBN 0-86577-584-2
 Central position in energy and
intermediary metabolism

 regulation of blood concentration of many

metabolites
 regulation of storage and production of energy
 synthesis of molecules for other tissues
 interconversion of nutrients
 storage of some substances
 formation and secretion of bile
Glucose in the liver can be

a) transformed to fatty acids

b) stored in glycogen molecules
c) oxidized to acetyl-CoA
d) used for production of NADPH
Metabolism of saccharides

 glucostatic function of the liver

 glycogen synthesis, glycolysis
 glycogen degradation, gluconeogenesis
 glucokinase, glc-6-phosphatase
 pentose cycle
 Cori cycle and glucose-alanine cycle
Metabolism of saccharides (II)

 excess of glucose  FFA  TAG

 transformation of saccharides to glucose
 metabolism of fructose (fructokinase)
 synthesis of amino saccharides
 synthesis of uronic acids
 degradation of insulin and glucagon
The figure was adopted from http://connection.lww.com/Products/porth7e/documents/Ch40/jpg/40_004.jpg (April 2007)
Fatty acids entering the liver can be

a) used for synthesis of TAG

b) transformed to glucose
c) transformed to ketone bodies
d) oxidized to CO2 and H2O
Metabolism of lipids
 liver controls blood FFA concentration
 energy is produced mainly by -oxidation
 synthesis of ketone bodies
 synthesis of TAG (from FFA, glc, AA)
 synthesis of cholesterol
 synthesis of bile acids
 synthesis of phospholipids
 synthesis of VLDL and HDL
 degradation of plasma lipoproteins
The figure is from: Color Atlas of Biochemistry / J. Koolman, K.H.Röhm. Thieme 1996. ISBN 0-86577-584-2
The figure was adopted from http://connection.lww.com/Products/porth7e/documents/Ch40/jpg/40_006.jpg (April 2007)
Choose the correct statement(s) about
the metabolism of lipoproteins in the
liver:

a) the hepatocyte synthesizes

chylomicron particles
b) triacylglycerols leave the liver
incomporated in VLDL
c) apoproteins are synthesized in the
liver
d) LDL transports cholesterol from
peripheral tissues to the liver
 Amino acids in the liver can be

a) used for synthesis of clotting factors

b) used for synthesis of immunoglobulins
c) transformed to glucose (only glucogenic
amino acids)
d) decomposed, urea is one of the main
products
Metabolism of N-containing compounds
 synthesis of plasma proteins (except Ig)
 synthesis of coagulation factors
 synthesis of acute phase reactants
 degradation of amino „N“ (urea, Gln)
 synthesis of nonessential amino acids
 metabolism of aromatic AAs
 degradation of purines to uric acid
 synthesis of creatine
 conjugation and excretion of bilirubin
The figure was adopted from http://connection.lww.com/Products/porth7e/documents/Ch40/jpg/40_005.jpg (April 2007)
 HOOC COOH

Bilirubin
O N N N N O
H H H H

a) belongs among linear tetrapyrrols

b) is excreted mainly with bile
c) is soluble in water after its
conjugation, e.g. with glucuronic acid
d) is called „direct bilirubin“ if it is
bound to albumin
The figure is from: Color Atlas of Biochemistry / J. Koolman, K.H.Röhm. Thieme 1996. ISBN 0-86577-584-2
 excretion

The figure was adopted from http://connection.lww.com/Products/porth7e/documents/Ch40/jpg/40_007.jpg (April 2007)

 Causes of
hyperbilirubinemia

1) increased bilirubin
formation

2) decreased bilirubin
uptake by hepatocyte

3) deficit in conjugation

4) defect of active
transport to bile

5) biliary obstruction

The figure was adopted from the book: Klinická biochemie - požadování a hodnocení BCH vyšetření /
J. Masopust (Karolinum 1998)
 BILI in BILI in UBG in UBG in
cause jaundice
serum urine urine feaces

prehepatic hemolytic  indirect no  

 both:
hepatic liver indirect yes  
and direct

posthepatic obstructive  direct yes no no

indirect = unconjugated = insoluble in water (= fat soluble) = bound to albumin

direct = conjugated = soluble in water
Metabolism of vitamins

 provitamins vitamins, storage of vitamins

 carotenes  vitamin A
 25-hydroxylation of provitamin D (→ calcidiol)
 cleavage of side chain of vitamin K
 storage of vitamin B12
 synthesis of nicotinic acid from Trp
 formation of coenzymes from B vitamins
 Metabolism of minerals

 storage of iron (ferritin)

 storage and metabolism of other trace elements
(Cu, Mn, Co, Mo, Zn,..)
 synthesis of transport proteins
(transferrin, ceruloplasmin)
 deiodation of thyroidal hormones → I- (iodide)
Metabolism of hormones
 degradation and excretion
(see 3rd semester)

Metabolism of xenobiotics
 see next seminar
 Metabolic
pathways in
different zones
of the liver
lobule

The figure was adopted from

http://www.tharu.com/academic/html/newcastle/liver.htm
(April 2007)
a) periportal hepatocytes - higher pO2:

 more mitochondria, less ER

 blood contains a lot of O2 and nutriens
 more of oxidative reactions
 antioxidative defense (glutathion)
 CC, RCH, oxidative phosphoryl., -oxidation
 urea synthesis
 glukoneogenesis
 cholesterol synthesis
 proteosynthesis
b) perivenous hepatocytes - lower pO2:

 blood contains few O2 and nutriens

 more of reductive reactions
 synthesis of lipids
 glycogen synthesis
 ketogenesis
 biotransformation of xenobiotics (sm. ER)
 detoxification of NH3: synthesis of Gln
 Glutamine
cycle
in the liver

The figure was adopted from: Devlin, T. M. (editor): Textbook of Biochemistry with Clinical Correlations, 4th ed. Wiley ‑Liss, Inc.,
New York, 1997. ISBN 0‑471‑15451‑2
Choose the mtb pathway(s) proceeding
only in the liver:

a) gluconeogenesis
b) ketogenesis
c) synthesis of urea
d) synthesis of bile acids
Choose correct statement(s) about
enzymes of hepatocytes

a) ALT participates in a metabolism

of amino acids
b) ALP belongs among esterases
c) LD needs NADH as a coenzyme
d) AST catalyzes one of reactions
of a pentose cycle
Liver tests
 total bilirubin (‹ 22 M)
 ALT (‹ 0,75 kat/L)
 AST (‹ 0,75 kat/L)
 ALP (‹ 2,29 kat/L)
 GMT (men: 0,25-1,77, women: 0,17-1,10 kat/L)

the values are used in FNKV

IV Biliary secretion

128
 Structure/Function of Liver
Liver lobule

Central
vein Central
vein

Bile
Blood

Bile
canaliculus

Portal
triad
Hepatic
artery

Hepatic
portal vein 129
Portal triad
130
 Secretion and storage of bile

Constituents of bile Liver Gallbladder

Water 98% 92%
Bile salts 1% 6%
Bilirubin( 胆红素） 0.04% 0.3%
Cholesterol （胆固醇） 0.1% 0.3-0.9%
Fatty acids 0.12% 0.3-1.2%
Lecithin （卵磷脂） 0.04% 0.3%
Na, K, Ca, Cl, HCO3

131
 Functions of bile
Emulsification of fats
Increased absorption of lipids into
enterocytes (include vitamin A, D, E, K)
Increased synthesis and secretion of bile
Cholesterol excretion (only route)
Excretion of breakdown products of
haemoglobin (bilirubin ，胆红素 ) 132
(a)
A molecular model of a
bile salt, with the
cholesterol-derived “core”
in yellow.

(b)
A space-filling model of a
bile salt.
The non-polar surface
helps emulsify fats,
The polar surface
promotes water solubility.
133
Of the 6 components present in
bile, only Bile salts and
phospholipids aid in digestive
processes.

Bile salts and phospholipids

convert large fat globules into
smaller pieces with polar
surfaces that inhibit re-
aggregation.

emulsification

134
Emulsified fat globules are small
enough
that lipase enzymes gain access
to degrade triglycerides to
monoglycerides and fatty acids,

Monoglycerides and fatty acids

enter the absorptive cells by
simple diffusion
or aggregate to form loosely held
micelles, which readily break
down.
135
Regulation of bile secretion and empty of
gallbladder

1. Nervous regulation: Vagus-vagus reflex

2. Humoral regulation: CCK , Gastrin, Secretin, SS

3. Bile salt: Enteroheptic circulation (Def.)

136
 In fasting state
Bile stored in gall bladder& concentrated
Liver
Aqueous secretion from duct
epithelium rich in HCO3- and
HCO3- stim. by secretin

HCO3-

Cl-
Na+
H2O
Sphincter of Oddi
Fluid & electrolytes
absorbed by active
(closed)
transport of Na+ 137
 Digestion - fat in
duodenum stimulates
CCK release from I
cells

FAT
CCK

Gall bladder
contraction BILE

Sphincter of Oddi relaxes138

 Liver - The enterohepatic
secretion circulation

Portal vein

Gallbladder-storage
Common
& concentration
bile duct

Duodenum-digestion & Ileum - absorption of

emulsification bile acids
139
Up to 95% of the
cholesterol-based bile salts
are “recycled” by
reabsorption along the
intestine.

Inhibition of reabsorption
results in synthesis of new
bile acids and lowering of
cholesterol levels.

Increasing dietary fiber

could trap a greater
percentage of the bile in the
fibrous feces. 140
 Regulation of Bile Release
 Acidic, fatty chyme causes the duodenum to release:
 Cholecystokinin (CCK) and secretin into the bloodstream
 Bile salts and secretin transported in blood stimulate the liver to
produce bile
 Vagal stimulation causes weak contractions of the gallbladder
 Cholecystokinin causes:
 The gallbladder to contract
 The sphincter of Oddi to relax
 As a result, bile enters the duodenum

141
Small Intestine secretion

142
 Composition and function
Digestive enzymes not secreted from small intestine -
from pancreas or found on enterocytes
except enterokinase secreted from duodenal
mucosa
Mucus/alkali secretions - mucosal protection
Aqueous secretions
Function
Lubricate and protect intestinal surface (Ig A)
Dilute digestive products
Digest specific food substances
143
(enzymes in enterocytes: peptidase, sucrase, etc )
 Regulation of small intestinal
secretion
Local stimuli
The presence of chyme in the intestine
Hormonal regulation
Secretin
CCK
Neuronal regulation
Vagus nerve – excitatory
Sympathetic nerve - inhibitory
144
 EMPEDU

SUSUNAN
1. NATRIUM BIKARBONAT, NATRIUM CHLORIDA
2. ASAM EMPEDU
PRIMER : ASAM KOLAT, ASAM KENODEOKSI KOLAT
SKUNDER : ASAM DEOKSI KOLAT
ASAM LITHO KOLAT
3. LESITIN
4. KOLESTEROL
5. PIGMEN EMPEDU (BILIRUBIN)
6. PROTEIN
7. HASIL METABOLISME DAN SEKRESI HATI, SEPERTI HASIL
DETOKSIKASI OBAT
 FUNGSI EMPEDU

1. Emulsifikasi,
Menurunkan tegangan permukaan
mengemulsikan lemak
2. Menetralkan asam
3. Eksresi,
Eksresi asam empedu dan kolestrol
mengeluarkan racun, obat, dll
2. Kelarutan kolesterol
3. Metabolisme pigmen empedu (bilirubin)
Gambar 1.7. Pencernaan dan penyerapan triasilgkiserol. FA= asam lemak rantai panjang.
(Sumber: Mayes P.A.,1988)
 BATU EMPEDU (GALSTONE)

 EMPEDU SANGAT JENUH DENGAN KOLESTEROL

 INFEKSI MENGENDAPKAN KOLESTEROL SEBAGAI
KRISTAL
 TERBENTUK BATU

PENYEBAB:
 SINTESIS KOLESTEROL HATI MENINGKAT

 SINTESIS ASAM EMPEDU MENURUN

(MENURUNNYA AKTIFITAS 7 ∝- HIDROKSILASE)

 IKATAN PEPTIDA;KONYUGASI

O
OH GLISIN pKa =3,7
O
12 C
OH H N CH2 C O
TAURIN pKa =1,5
H OR
3 7
HO OH
H N CH2 CH2 SO2O-

H
ASAM KOLAT (Asam Empedu Primer)

Tidak ada OH pada Atom C12=Asam Kenodeksikolat (primer)

Tidak ada OH pada Atom C7=Asam Deoksiklat (sekunder)
Tidak ada OH pada Atom C7 dan12 = Asam Lithokolat (sekunder)

Gambar 1.8. Susunan asam empedu, asam empedu dikonyugasi dengan glisin
atom taurin dengan keluarnya air membentuk suatu ikatan peptida. Konstanta
ionisasi atau glikokolat dan taurokholat terlihat pada bagian kanan. (Sumber :
Davenport, H. W., 1984
gambar 1.9. gambaran mengenai tiga komponen utama empedu
(garam empedu, fosfatidil kolin, dan kolesterol) pada koordinat segi
tiga. Tiap komponen dinyatakan dalam presentase “mol” garam
empedu total, fosfatidil kolin, dan koesterol. Garis ABC merupakan
kelarutan maksimum kolesterolpada beberapa macamgaram empedu
dan fosfatidil kolin. Titik P melukiskan komposisi normal empedu yang
mengandung 5% kolesterol, 15% fosfatidi kolin dan 80% garam
empedu, komposisi ini terletak pada daerah fase tunggal cairan misel.
Bila komposisi empedu diatas garis ABC, menggambarkan bahwa
kolesterol dalm bentuk sangat jenuh atau prespitasi.

(sumber : Mayes, P.A., 1988)

gambar. 1.10. Sirkulasi enterohepatik asam
empedu. Sintesis di hati, disimpan di kandung
empedu, penyerapan pasif, dan aktif di usus
halus, sebagian kecil melalui usus besar,
penyerapan pasif dalam usus besar, dan ekskresi
melalui fases. Asam empedu yang diserap
kembali kehati melalui darah porta.
Digestion and absorption of
lipids
 Abnormalities of lipids
digestion
1. Pancreatic insufficiency (chronic pancreatitis and
cystic fibrosis)
2. Acidity of duodenal content (zollinger-Ellison
syndrome)
3. Deficiency of bile salts (ileal resection)
4. Bacterial over growth (deconjugation of bile salts)
5. Decrease intestinal cells for absorption
6. Failure of synthesis of apoproteins
(abetalipoproteinemia)
Digestion and absorption of
carbohydrates
Carbohydrate malabsorption
 Lactose malabsorption syndrome
 Symptoms
- gurgling noises in the intestine
- flatulence
- diarrhea
 Sucrase-isomaltase deficiency
- decrease level of sucrase
- suppression of transporter protein

 Glucose-galactose malabsorption syndrom

- deficiency in transporter protein
Digestion and absorption of
proteins
Vitamins and Electrolytes
transport and Diarrhea
Dr. Alzoghaibi
Absorption of vitamins
 In terms of absorption, vitamins are classified
to whether they are lipid-soluble or water-
soluble
 The fat-soluble vitamins include A, D, E, & K
 The water-soluble vitamins are C, B1, B2, B6,
B12, and folic acid
Absorption of vitamins (cont)
A. Fat-soluble vitamins are incorporated into
micelles and absorbed along with other lipids
B. Most water-soluble vitamins are absorbed by
Na-dependent cotransport mechanisms
C. Vitamin B12 is absorbed in the ileum and
requires intrinsic factor
 Gastrectomy results in the loss of parietal cells and loss
of intrinsic factor pernicious anemia
Absorption and secretion of
electrolytes and water
 Electrolytes and H2O may cross intestinal
epithelial cells by either cellular or
paracellular
 The permeability of the tight junctions varies
with the type of epithelium
o A tight epithelium is the colon
o Leaky epithelia are the small intestine and
gallbladder
Absorption and secretion of
electrolytes and water
 Absorption of NaCl:
Na moves into the intestinal cells by the
following mechanisms
1) Passive diffusion

2) Na-glucose or Na-amino acid cotransport

3) Na-Cl exchange

4) Na-H exchange
Absorption and secretion of
electrolytes and water
 Cl absorption accompanies Na absorption by
the following mechanisms:
1) Passive diffusion
2) Na-Cl cotransport
3) Cl-HCO3 exchange
 Absorption and secretion of K
 K is absorbed in the small intestine by passive diffusion
 K secretion in the colon is stimulated by aldosterone
 Excessive loss of k in diarrheal fluids causes hypokalemia
Heme transport
Ca Absorption by Enterocytes

 plasma Ca parathyroid hormone

25-hydroxy-vitamin D3 kidney

1,25 dihydroxy-vitamin D3
Stimulates synthesis of Ca-binding protein and
Ca-ATPase in enterocytes
 Diarrhea
 Diarrhea
 To run through 
  ECF   arterial pressure
  HCO3 (relative to Cl)  Hyperchloremic metabolic
acidosis
  K  Hypokalemia

Causes of Diarrhea:
 Decreased surface area for absorption
 Osmotic diarrhea (lactase deficiency)
 Secretory diarrhea
Hormonal control of absorption &
secretion
 Glucocorticoid = absorption of H2O & ions
(small & large intestine)
 Catecholamines = intestinal secretion

 Somatostatin = H2O & ions absorption

(ileum & colon)
 Epinephrine = NaCl absorption (ileum)

 Aldosterone = synthesis of Na channel (colon)

HASIL AKHIR PENCERNAAN

KARBOHIDRAT : MONOSAKHARIDA (GLUKOSA, GALKTOSA DAN

FRUKTOSA)

PROTEIN : ASAM AMINO DAN DIPEPTIDA

TRIASILGLISEROL (LEMAK TRIGLISERIDA) :

ASAM LEMAK, GLISEROL DAN MONOASIL GLISEROL (MONOGLISERIDA)

ASAM NUKLEAT : NUKLEOBASA, NUKLEOSIDA DAN PENTOSA

MAKANAN SERAT : TIDAK DICERNA OLEH ENZIM (MANUSIA)

 HASIL AKHIR PENCERNAAN

Protein Peptida Enzim Metode Pengaktifan Substrat Hasil akhir

Dan Kondisi Optimum atau Fungsi
Sumber Sekresi Dan Pengaktifan
Rangsang Sekresi

Kelenjar liur: Mensekresi Amilase liur Ion Khlorida penting Pati Glikogen Maltose
saliva sebagai respon pH 6,6-8,8 tambah 1:6
refleks terhadap adanya glukosida
makanan dalam rongga (oligosakarid
mulut a) tambah
maltotriosa

Kelenjar Lingualis Lipase lingualis Rentang pH: 2,0- Ikatan ester Asam lemak
7,5;optimum: 4,0-4,5 primer rantai tambah 1,2-
pendek pada sn-3 diasilgliserol

Kelenjar Lambung: Pepsin A Pepsinogen Protein Peptida

Sel chief dan parietal (fundus), dikonversi menjadi
mensekresi getah lambung Pepsin B pepsin aktif oleh
sebagai tanggapan (pilorus) HCL, pH 1,0-2,0
terhadap rangsang refleks,
dan kerja gastrin

Renin Kalsium penting Kasein susu Mengkoagul

untuk aktivitas, pH asikan susu
4,0
Pankreas : Tripsin Tripsinogen Protein Peptida Polipeptida
Keberadaan dikonversi menjadi dipeptida
chyme asam tripin aktif oleh
dari enterokinase usus
lambung halus pada pH 5,2-
mengaktifka 6,0, autokatalitik
n duo-
Khimotripsin Disekresikan Protein Peptida Sama seperti
denum
sebagai Tripsin, berdaya
untuk
khimotripsinogen Koagulan susu
menghasilka
dan diubah menjadi yang lebih besar
n:
bentuk aktif oleh
tripsin, pH 8,0
1) Sekretin,
Elatase Disekresikan Protein Peptida Polipeptida
yang secara
sebagai Dipeptida
hormonal
proelastase dan
merangsang
diubah menjadi
aliran getah
bentuk aktif oleh
pankreas.
tripsin
2)
Kolesistokini Karbosipeptidse Disekresikan Polipeptida pada Peptida pendek.
n, yang sebagai ujung karboksil Asam Amino
merangsang prokarboksipeptida bebas pada Bebas
prodeksi se, yang diaktivkan rantainya
enzim oleh tripsin
Amilase pH 7,1 Pati Glikogen Maltose tambah
Pankreatik 1:6 glukosida
(oligosakarida)
tambah
maltotriosa
 HASIL AKHIR PENCERNAAN
  Lipase Diaktifkan oleh Ikatan ester primer Asam lemak
garam empedu, pada triasilgliserol monoasilgliserol,
fosfolipid, kolipase diasigliserol,
gliserol

Ribonuklease   Asam Ribonuklease Nukleotida

Deoksiribonuklease   Asam Nukleotida

Deoksiribonukleat

Hidrolase ester Diaktifkan oleh Ester Kolesterol bebas

kolesteril garam empedu Kolesteril tambah asam
lemak

Fosfolipase Disekresikan sebagai Fosfolipid Asam lemak,

A2 proenzim, diaktifkan lisofosfolipid
oleh tripsin, dan
Ca2+

Hati dan kandung (Garam empedu, dan   Lemak juga Garam Empedu
empedu: alkali) menetralkan Khime Asam lemak
Kolesistokinin, Asam mengkonjugat, dan
hormon dari mukosa mengemulsihaluska
usus halus-dan
n misel garam
mungkin juga
empedu lemak
gastrin,dan sekretin-
merangsang kandung netral, dan liposom
empedu dan sekresi
empedu oleh hati
 HASIL AKHIR PENCERNAAN
Usus halus: Amino-   Polipeptida pada Peptida pendek,
Sekresi kelenjar peptidase ujung amino bebas asam amino bebas
Brunner pada rantainya
duodenum,dan
Kelenjar Liberkhun
  Dipeptidase   Dipeptida Asam Amino

Sukrase pH 5,0-7,0 Sukrosa Fruktosa, glukosa

Maltase p H 5,8-6,2 Maltosa Glukosa

Laktase pH 5,4-6,0 Laktosa Glukosa, Glaktosa

Trehalase   Trehalaso Glukosa

Fosfatase pH8,6 Fosfat organik Fosfat bebas

Isomaltase atau 1:6   1:6 glukosida Glukosa

glukosidase

Polinukleotidase   Asam nukleat nukleotida

Nukleosidase   Nukleosida purin Basa purin atau

(fosforilase atau primidin pirimidin, pentosa
nukleosida) fosfat
Gambar 2.1. Susunan Pati (starch). Pemecahan oleh
amilase pankreas terjadi pada ikatan ∝-1,4 dan sebagai
hasil hidrolisis merupakan rantai lurus Oligosakarida.
Karena amilase pankreas tidak menghidrolisis ikatan ∝-
1,6, maka isomaltose juga merupakan hasil hidrolisis.
Hidrolisis lebih lanjut oleh enzim maltase dan
isomaltase pada brush border sel epitel usus.
(sumber: Devenport, H.W., 1984)
Gambar 2.2. Skema yang menggambarkan penyerapan glukosa oleh sel epitel usus
bersamaan dengan pengangkatan Na +, dan terjadinya selisih elektrokimia Na +.
(Sumber: Davenport, H.W.,1984
PENCERNAAN KHO :

MULUT
STARCH AMILASE MALTOSA
KANJI LUDAH MULUT MALTOTRIOSA
DEXTRIN
USUS
KANJI ISOMALTASE
GLUKOSA
MALTOSA AMILASE PANKREAS

SUKROSA SUKRASE GLUKOSA

(GULA TEBU) +
FRUKTOSA

GLUKOSA
LAKTOSA LAKTASE
+
(GULA SUSU)
GALAKTOSA
Gambar 2.3. Proses pencernaan, dan penyerapan lemak
Gambar 2.4. Pencernaan dan penyerapan nukleoprotein. (Sumber: Davenport,
H.W.1982)
 Tabel 2.1. Penyerapan Beberapa Vitamin

VITAMIN LARUT DALAM LEMAK,

Larutan dalam misel dibutuhkan untuk penyerapan :
A Retinol (MW 286), karoten Dapat jenuh, difusi diperantarai
pengemban
(MW 537)
D Kalsiferol (MW 397) dan Difusi pasif
Kongener
E ∝-Tokoferol (MW 431 Difusi Pasif
K Vitamin K (MW 451) Difusi Pasif
Menadion (MW 172)

VITAMIN LARUT DALAM AIR :

B1 Tiamin (MW 301), tiamin Transpor aktif dan difusi
Pirofosfat (MW 479)
B2 Ribovlavin (MW 376) Difusi saja (?)
B3 Asam Nikotinat (MW 123) Difusi Saja
Nikotamida (MW 122)
B5 Asam Pantotenat (MW 219) Difusi Saja
 Tabel 2.1. Penyerapan Beberapa Vitamin

B6 Piridoksal (MW 167) Difusi saja

Dan Kongener
B12 Sianokobalamin
(MW 1,355) dan Konjugat
Bc Asam Folat (MW 441), dan
monolutamil-Konjugat
C Asam askorbat (MW 176)
H Biotin (MW 244)
Bergabung dengan Faktor Intrinsik dari
lambung, diserap melalui pinositosis
pada ileum terminalis. Jika faktor
intrinsik tidak ada, maka diserap dalam
jumlah mikrogram
bila dimakan dalam beberapa miligram
Konjugat dihidrolisasi menjadi
folat, sebelum penyerapan aktif
diserap melalui transporaktif
bergantung Na+, tambah difusi
transpor aktif

Vitamin larut dalam lemak diserap seperti lemak yang lain. Didalam
lumen usus, vitamin ini larut dalam misel yang disusun oleh
monosiglerida, asam lemak bebas, dan garam empedu. Misel
membawa vitamin melalui unstirred layer ke permukaan mukosa,
kemudian Vitamin diserap secara difusi pasif melalui membran lipid sel
epitel. (Sumber: Davenport, H.W. 1984)
TABEL 3.1. PENGARUH GASTRIN, CCK, DAN SEKRETIN PADA SALURAN
PENCERNAAN*

GASTRIN
MENINGKATKAN TEKANAN ISTIRAHAT PADA
SFINGTER ESOFAGUS INFERIOR
PENTING : MERANGSANG SEKRESI ASAM OLEH SEL OKSINTIK
YANG SELANJUTNYA MERANGSANG SEKRESI
PEPSINOGENOLEH SEL CHIEF MELALUI REFLEKS
LOKAL
PENTING : MENINGKATKAN MOTILITAS ANTRUM GASTER
SEDIKIT MERANGSANG SEKRESI ENZIM DAN
BIKARBONAT OLEH PANKREAS, KONTRAKSI
KANDUNG EMPEDU
PENTING : MEMPUNYAI EFEK TROFIK PADA MUKOSA GASTER
TABEL 3.1. PENGARUH GASTRIN, CCK, DAN SEKRETIN PADA SALURAN
PENCERNAAN*

KOLESISTOKININ
SEDIKIT MERANGSANG SEKRESI ASAM LAMBUNG
PENTING : SECARA KOMPETITIF MENGHAMBAT SEKRESI ASAM
YANG DIRANGSANG OLEH GASTRIN
PENTING : KUAT MERANGSANG SEKRESI ENZIM OLEH PANKREAS
SEDIKIT MERANGSANG SEKRESI BIKARBONAT OLEH
PANKREAS, WALAUPUN DEMIKIAN
PENTING : KUAT MENINGKATKAN EFEK SEKRETIN DALAM
MERANGSANG SEKRESI BIKARBONAT OLEH PANKREAS
PENTING : KUAT MERANGSANG KONTRAKSI KANDUNG EMPEDU
MERANGSANG SEKRESI DAN MOTILITAS DUODENUM
MEMPERLAMBAT PENGOSONGAN LAMBUNG
PENTING : MEMPUNYAI KERJA TROFIK PADA PANKREAS
TABEL 3.1. PENGARUH GASTRIN, CCK, DAN SEKRETIN PADA SALURAN
PENCERNAAN*

SEKRETIN
MERANGSANG SEKRESI PEPSINOGEN
PENTING: MERANGSANG SEKRESI BIKARBONAT OLEH
PANKREAS, DAN HATI; SINERGISTIK DENGAN
CCK
PENTING: MENGHAMBAT SEKRESI ASAM YANG
DIRANGSANG OLEH GASTRIN
PENTING: MENGHAMBAT MOTILITAS GASTER DAN
DUODENUM MENGHAMBAT SFINGTER ESOFAGUS
INFERIOR MEMPUNYAI EFEK METABOLIK MIRIP
DENGAN GLOKAGEN

Sumber: Davenport, H.W,. 1987.

Gambar 2.5. Mekanisme pengangkutan Na dan cairan melalui lapisan sel
epitel pada mukosa usus ahlus, pada sel epitel usus, pompa Na, dan Cl tidak
berhubungan. Perbedaan tekanan osmotik antara membran lateral sel akan
menyebabkan pengaliran air. (Sumber: Davenport, H.W., 1984)
Gambar 2.7. Penyerapan dan ekskresi besi didalam usus
halus. (Sumber: Davenport, H.W.,1982)
INTOLERANSI LAKTOSA

TIMBULNYA GEJALA-GEJALA PADA SALURAN

PENCERNAAN ATAU MEMINUM BAHAN-BAHAN
MENGANDUNG LAKTOSA ATAUPUN HASIL OLAHANNYA.

GEJALA-GEJALA:
NYERI PERUT
DIARE
FLATULEN
GEMBUNG
Gambar 4.1.Patofisiologi diare akut pada malabsorpsi laktosa di usus halus
TABEL 4.1. PREVELENSI DEFISIENSI LAKTASE PADA BEBERAPA
POPULASI DI DUNIA
Australia (Kulit Putih) 10 %

Amerika Utara : - Kulit Putih 5-20 %

- Kulit Hitam 70-75%

Afrika (Bantu) 50 %

Denmark 5%

Asia : - Thailand 97 %
- India 55 %
- Jepang 90 %

Meksiko 74 %

Israel : - Yahudi 61 %
- Arab 81 %
TABEL 4.2. PENYEBAB DEFISIENSI LAKTASE SEKUNDER
1. BAYI PREMATUR
2. PASCA INFEKSI DAN INFESTASI
- GASTROENTERITIS AKUT
- GIARDIASIS
- SALMONELOSIS
- ESCHERICHIA COLI
- INFESTASI CACING
3. KEKURANGAN KALORI PROTEIN (KKP)
4. PASCA OPERASI GASTROINTESTINAL PADA BAYI
5. OBAT-OBAT SEPERTI : NEOMYCIN, ANTINEOPLASMA
6. GLUTEN-SENSITIVE ENTEROPATHY
Gambar 4.2. Penyebab intoleransi laktosa
 GLUTEN SENSITIVE ENTEROPATHY

KERUSAKAN MUKOSA USUS HALUS PADA ORANG YANG PEKA SESUDAH

MEMAKAN MAKANAN MENGANDUNG PROTEIN GLUTEN

LESI PADA MUKOSA:

 VILLUS DATAR

 SEL EPITEL BERBENTUK KUBUS

 INFILTRASI LIMFOSIT DAN SEL PLASMA

KEDALAM LAMINA PROPRIA

GEJALA:
MALABSORBSI PROTEIN, LEMAK DAN KARBOHIDRAT
MEMASUKI
USUS BESAR PATI SELUIOSA
HEMISELULOSA

DIMETABOLISASI OLEH HEKSOSA

BAKTERI UNTUK
PENTOSA
PERTUMBUHAN BAKTERI
GLIKOLISIS
LINTASAN
PENTOSA
PIRUVAT

PROSES ASETAT
AKHIR
PROPIONAT HIDROGEN
BUTIRAT METANA
KARBONDIOKSIDA

HASIL
AKHIR KELUAR KE KELUAR MELALUI
DIABSORBSI OLEH FESES UDARA PERNAPASAN
USUS HALUS DAN
SETELAH ABSORBSI
DIMETABOLISASIKAN

Gambar 5.1. Pemecahan karbohidrat didalam usus besar manusia

GAS DALAM SALURAN PENCERNAAN

1. MENELAN
2. FERMENTASI
3. NETRALISASI
HCl (LAMBUNG)+BIKARBONAT (PANKREAS) CO2
ASAM ORGANIK + BIKARBONAT
4. DIFFUSI
N2 DARI DARAH
Gambar 5.2. Metabolisme amonia, menunjukkan bahwa pengobatan hiperamonia dengan
diet rendah protein, pemberian antibiotik untuk mengurangi bakteri mengandung urease,
disamping itu pemberian laktulosa. Kira-kira separuh dari usus halus. Amonia dihasilkan oleh
banyak jaringan termasuk ginjal
Tabel 5.1. Kelainan pada pencernaan dan penyerapan lemak penyebab
steatorrhea

TAHAP GANGGUAN FISIOLOGIS STATUS MORBUS

Emulsifikasi Emulsifikasi Terganggu Difisiensi asam empedu

Trigliserida konjugasi;keasaman khime
usus halus yang berlebihan

Hidrolisis Defisiensi Lipase pankreatik Penyakit Pankreatik

Defisiensi bikarbonat relatif Penyakit Pankreatik atau
atau absolut hipersekresi gastrik

Pembentukan Defisiensi asam empedu Fistula Bilier atau sumbatan

Misel Konjugasi; defisiensi bilier; penyakit ileum atau
bikarbonat absolut atau reseksi ileum; dekonjugasi
relatif bakteri; penyakit Pankreatik
atau hipersekresi gastrik
Tabel 5.1. Kelainan pada pencernaan dan penyerapan lemak penyebab
steatorrhea
TAHAP GANGGUAN STATUS MORBUS
FISIOLOGIS

Penyerapan Penurunan ambilan sel; Reseksi usus halus atau

2-monogliserida pengurangan jumlah sel, pintas usus halus;
aktifias, atau luas tropical sprue atau
permukaan transpor kilo-mikron
  Kegagalan sintesis
Sel dijenuhkan oleh asam trigliserida,
lemak dan monogliserida pembentukan kilo
  mikron, atau transpor
  kilo mikron
 
Masa kontak memendek Masa transit memanjang
Pembentukan kilomikron Defisiensi pembentukan - lipoproteinemia
kilomikron

Transpor kilomikron Obstruksi limfatik atau Limfosarkoma;

Dari sel melalui limfa ke limfangiektasia lipodistrofi usus halus;
darah enteropati hilang protein