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An insight into multifunctional tool box: Akkermansia

muciniphila provides dynamic benefits to the
human gut
Downloaded from http://journals.lww.com/revmedmicrobiol by V0M3eMr08MG7uRhx2HJZ0/FHjJYEWcIOKA7zR1AWeDHfGf5yKxZxvFbgPdPAymQYqUVf28aAof2OieOrNJ7Ke767CO7ANLoyv4VWSvJDvYhuKWNPjJce2LUKpF3/pbTsgTdCO2e1Dk6zC93TzBle4MOqzXzeJXqvZ1RpoAfi80QR2ZzcD30kEzfPUhZjd/d/zkAPKn/SDBQ= on 02/01/2022

Kartikeya Tiwari

Akkermansia muciniphila is a mucin degrader that plays a major role in the human gut.
Multiple studies have shown that the level of abundance of this organism in the human
body is inversely related to diseases, such as diabetes, obesity and inflammatory bowel
disease. This organism has abilities to regulate the intestinal permeability, gut barrier
and inflammatory responses in various metabolic disorders by activating various
transcription factors and enhance the expression of receptors (TLRs, NLRs). Pangenome
of A. muciniphila provides comprehensive detail and role of encoding genes in
mitigation of metabolic dysbiosis. The present review discusses and summarizes the
role of A. muciniphila in diabetes mellitus type 2, obesity, nonalcoholic fatty liver
disease and other metabolic disorders.
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Reviews and Research in Medical Microbiology 2022, 33:000–000

Keywords: Akkermansia muciniphila, gut barrier, intestinal epithelium,

probiotics, toll-like-receptors

Introduction processes [4]. This organism belongs to phylum Verruco-

Our gastrointestinal tract hosts an environment for the
various kinds of microorganisms, which is involved in
many metabolic, nutritional, physiological and immuno-
logical functions. In the past decade, it has been evidently
proved that gut microbiota has an important role in
determining the well being of our health. One of the
organisms in the colonic mucosa-associated microbiota is
Akkermansia muciniphila (AKM), which colonizes a
considerable part of the human population and make up
1–4% of the fecal microbiota of normal adults [1]. AKM is
a Gram-negative, oval shaped, nonspore former, aero-
tolerant, anaerobic bacterium [2,3]. This organism was
discovered in 2004 serendipitously at Wageningen
University of Netherlands, when the research group was
searching for a new mucin-degrading microbe in human
faeces [2]. According to European Research Council,
initially A. muciniphila was identified and isolated by
Professor Willem deVos from Wageningen University, and
thereafter in 2007, Professor Patrice Daniel Cani
highlighted the behavior of this bacterium in metabolic
microbia (Fig. 1), and is discovered in the human gut [2]. It
is known as mucin-degrading bacterium as it uses solely a
source of carbon and nitrogen elements [2]. This organism
helps in maintaining a healthy protective barrier by
degrading the external mucus layer, which leads to
continuous renovation of mucosa and prevents entrance
of enteropathogens [5]. Therefore, because of its unique
characteristics, it has paved more scientific research focused
on this organism’s roles in down-regulating metabolic
disorders and strengthening the gut barrier (Fig. 2). AKM is
affected by nutrients in the mucus layer located nearby to
the intestinal epithelia [6]. Thus, the abundance of AKM is
negatively related to several diseases [1]. The population of
AKM is reduced in metabolic disorders, such as obesity and
type 2 diabetes mellitus (T2DM) (Fig. 3).
Recent developments on this bacterium compiled by
Zhang et al. in 2021 [7] described the potential of AKM in
inflammatory bowel disease and summarized the research
findings with specific key points: AKM shows anti-
inflammatory potential in inflammatory bowel disease;

Department of Microbiology, International Medical School, Management and Science University, Shah Alam, Selangor, Malaysia.
Correspondence to Kartikeya Tiwari, Professor, Department of Microbiology, International Medical School, Management and
Science University, Shah Alam, Selangor 40100, Malaysia.
E-mail: drkartikeyaa2zmicrobiology@gmail.com
Received: 11 September 2021; revised: 21 October 2021; accepted: 2 December 2021

DOI:10.1097/MRM.0000000000000305

ISSN 2770-3150 Copyright Q 2022 Wolters Kluwer Health, Inc. All rights reserved. 1
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Fig. 1. Taxonomic description of Akkermansia muciniphila bacterium.

the colitogenicity of AKM is context-dependent. Another important mechanism of A. muciniphila in mucin

Similarly, Zou and Chen [8] in 2020 described the use
of AKM against multiple diseases in their review and
discussed the possible ways of engineering the AKM
bacterium, so that the complete benefits can be
accomplished.
degradation, is the secretion of sulfate [9] by using sulfatase
enzyme [1]. This produced sulfate is utilized by sulfate-
reducing bacteria and converted into sulfide [10]. The
toxicity of hydrogen sulphide is minimized by the action of
A. muciniphila through this unique mechanism [11].

Symbiotic interaction of Akkermansia

muciniphila in the human gut
A. muciniphila is a part of the gut, which hosts a complex
and diverse microbiota. AKM interactions with other gut
bacteria has been explained in several studies. Mucin
degradation by A. muciniphila produces various com-
pounds, such as 1, 2-propanediol, propionate and acetate.
The acetate produced is further utilized by Anaerostipes
caccae, Eubacterium hallii and Faecalibacterium prausnitzii
bacteria. The combined effect of A. muciniphila and these
organisms showed enhanced butyrate production. In the
cascade reactions, the cofactor pseudo-vitamin B12 is
produced by E. hallii organisms. This cofactor pseudo-
vitamin B12 is utilized by A. muciniphila, plays a role in the
conversion of succinate to propionate [9].
Role of Akkermansia muciniphila in type 2
diabetes mellitus
A metagenome-wide association analysis of intestinal
microbiota in patients with T2DM suggests intestinal
dysbiosis and altered gut microbiota composition [12].
Multiple researches demonstrated that A. muciniphila
balances energy homeostasis by affecting gut barriers, which
is important for metabolic endotoxemia and metabolic
disorders. These findings raise the potential in future medical
fields for targeting gut microbiota in order to down-regulate
metabolic diseases and benefit human health [13].
T2DM is a very common endocrine and metabolic
disease [14]. Multiple molecular mechanisms of AKM are

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Akkermansia muciniphila provides benefits to the human gut Tiwari 3

Fig. 2. Akkermansia muciniphila and other probiotic bacteria interaction with intestinal epithelial barrier. Mucus secreted by
goblet cells, which protect the external intestinal layer from invading pathogens. The beneficial bacteria at the external surface of
the intestinal epithelial layer breaks down mucus and dietary fibers into SCFA, which provides energy to intestinal cells. MAMP of
probiotics recognized by PRRs, such as NLRs and TLRs and regulate IEC pathways, such as peroxisome proliferator-activated
receptor gamma (PPAR-g) and mitogen-activated protein kinases (MAPK) to initiate protection to intestinal epithelial layer. IEC,
intestinal epithelial cells; MAMP, microorganism-associated molecular pattern; NLRs, NOD-like receptors; PRRs, pattern
recognition receptors, SCFA, short-chain fatty acid; TLRs, toll-like receptors.

believed to contribute to down-regulating the metabolic
diseases and T2DM. Some of the potential mechanisms
are modulating inflammation, disruption of dietary
constituents, interruption of gut permeability, glucose
and lipid metabolism, insulin tolerance and overall energy
homeostasis in the mammalian host [15].
T2DM is associated with higher levels of pro-inflamma-
tory cytokines, chemokines and inflammatory proteins.
The harmful bacterial colonization and dysbiosis leads to
metabolic endotoxemia and low-grade inflammatory
conditions. For example, induction of interleukin-10 by
A. muciniphila plays a role in improvement of glucose
metabolism as over-expression of this cytokine in the
muscle protects from ageing-related insulin resistance
[14]. Dagdeviren and his co-workers observed Lactobacil-
lus, Bacteroides and A. muciniphila have been found to
suppress tumour necrosis factor (TNF) in order to inhibit
inflammation [1,16].
The immune system plays a significant role in balancing
between commensal and pathogenic bacteria. The
immune system of the healthy body not only eradicates
harmful bacteria but also helps in colonization of
beneficial bacteria. This homeostasis is established by
the activation of pattern recognition receptors (TLRs,
NLRs). AKM induces the cytokine production through
activation of Toll-like receptors 2 and 4, which will

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4 Reviews and Research in Medical Microbiology 2022, Vol 33 No 00
Fig. 3. Akkermansia muciniphila deficiency in various con-
ditions, such as diabetes and obesity lead to intestinal dys-
biosis, which results in increased gut permeability.
Weakened gut barrier allows translocation of bacterial com-
ponents, such as LPS into circulation and promotes metabolic
endotoxemia. This inflammation results in further organ injury
and increases complications, such as NAFLD, insulin resis-
tance and hyperlipidemia. AKM breaks down nondigestible
diet components and degrades mucin in the intestinal mucous
layer into energy source to cells. The metabolite (SCFA-
acetate, butyrate, propionate) and components of AmEVs,
recognized by PRRs (TLRs, NLRs) activates various transcrip-
tion factors (AMPK, FFARs) in regulating host metabolism and
strengthen gut barrier, and modulate intestinal permeability
by enhancing gene expression of gut tight junction proteins.
AKM, Akkermansia muciniphila; AmEVs, A. muciniphila-
derived extracellular vesicle; AMPK, adenosine monopho-
sphate-activated protein kinase; FFAR, free fatty acid recep-
tors; LPS, lipopolysaccharides; NAFLD, nonalcoholic fatty
liver disease; NLRs, NOD-like receptors; PRRs, pattern rec-
ognition receptors; SCFA, short-chain fatty acids; TLRs, toll-
like receptors.
regulate bacterial recognition, and they can also optimize
the host metabolism and improve intestinal barrier
function (Table 1).
Another feature of human T2DM is increased gut
permeability, this translocates intestinal microbial products
into the blood and causes metabolic endotoxemia [17].
Extracellular vesicle-coated A. muciniphila modulates gut
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permeability and enhances tight junction expression. This
expression is enhanced by AMPK activation in the gut
epithelium. The gut integrity is enhanced by Amuc_1100
modulation-based expression of occludin and tight
junction protein-1 [18]. The main factor behind this
modulation is up-regulated mRNA expression for the
synthesis of various types of tight junction of proteins [19].
AKM increases fatty acid oxidation, energy expenditure and
reduces fatty acid synthesis to cut down body fat mass. This
specific modulated pathway is to reduce obesity and T2DM
[18]. This organism increases the production of endocan-
nabinoid receptors agonists (Fig. 4), such as 2-arachido-
noylglycerol, 2-palmitoylglycerol, 2-oleoylglycerol to
enhance the anti-inflammatory effects, metabolic endotox-
emia and the stimulation of gut peptide (GLP-1 and GLP-
2), which helps in glucose homeostasis, respectively [20].
Latest study conducted by Depommier et al. [21] in 2019
found significant improvement in overweight and obese
human volunteers when supplemented with AKM for 3
months (Fig. 5). This study suggested the use of AKM in
pasteurized form instead of live form AKM to improve
the insulin sensitivity and significant fall in insulinemia.
Interaction of Akkermansia muciniphila
with lipid metabolism in obesity and
related diseases
The relationship between abundance levels of A.
muciniphila is inversely proportional to the body weight
of animals and humans [22]. The research work conducted
by Schneeberger and co-workers demonstrated that the
modulated gene expression in white adipose tissue in high-
fat diet (HFD) induced obesity in mice [23]. This leads to
profound changes in key genes implicated in inflammation,
fatty acid oxidation and lipogenesis [23].
Higher abundance level of A. muciniphila was found in
fecal samples from healthy individuals compared with
obesity and T2DM patients. However, diet intervention
was strongly believed to progressively improve the
abundance level of AKM [23]. Previous studies reported
that A. muciniphila convert the dietary fiber into acetate,
butyrate and propionate by degrading the mucin
protective layer in the colon as their carbon and energy
source. Furthermore, these short-chain fatty acid
(SCFAs) metabolites have been widely discussed
(Fig. 3) to have an important role in our gut system as
it has beneficial impact on lipid and glucose metabolism as
well as gut permeability [22]. Li and co-workers found
out in their research about an improvement in body
weight and fat mass in HFD mice after introducing
live and heat-killed A. muciniphila. They also discovered
the suppression of intercellular adhesion 1 (ICAM-1)
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Akkermansia muciniphila provides benefits to the human gut Tiwari 5

Table 1. Interaction of Akkermansia muciniphila within the gut of humans.

Receptors/co-receptors Role and action of Akkermansia muciniphila Study model Disorders/diseases References

PPARg SCFA lowers PPARg expression and this Male C57Bl/6J mice Obesity [11]
stimulates the UCP2-AMPK signaling
pathway. This shifts the lipid synthesis to
lipid oxidation and aids in lipid
dysregulation.
FFAR/GPR SCFA stimulates FFAR on L-cells of colon, Male C57BL6 mice Obesity and Diabetes [12]
releases GLP-1 and PYY. These hormones
aid in lipids dysregulation and glucose
metabolism.
Tight junction proteins Amuc 1100 increases mRNA expression of C57BL (Apoe-/-) mice - [13]
tight junction proteins (occludin, claudin 3).
Consequently, this improves gut barrier and
modulates intestinal permeability.
ICAM-1, MCP-1 and TNFa mRNA expressions of ICAM-1, MCP-1 and C57BL (Apoe-/-) mice Atherosclerosis [13]
TNFa are inhibited with the supplement of
AKM. This prevents adhesion of
macrophage onto endothelium and
subsequent transmigration into intima.
Gut TLR2/4 Amuc 1100 activates TLR2/4, which further Mice T2DM [14]
induces cytokine production. This
mechanism mediates immune homeostasis
in intestinal mucosa and improves gut
barrier.
Hepatic TLR4 Bacterial components (LPS) bind to hepatic Mice NAFLD [15,16]
TLR4 and activate inflammatory cascade.
AKM prevents inflammatory response by
suppressing SERBP gene and IL-6
expression.

AMPK, adenosine monophosphate-activated protein kinase; FFAR, free fatty acid receptor; GLP-1, glucagon like peptide 1; GPR, G-protein
receptor; ICAM, 1-intracellular adhesion molecule 1; IL-6, interleukin; LPS, lipopolysaccharides; MCP-1, monocyte chemoattractant protein 1;
NAFLD, nonalcoholic fatty liver disease; PPARg, peroxisome proliferator-activated receptor gamma; PYY, peptide tyrosine tyrosine; T2DM, type 2
diabetes mellitus; TLRs, toll-like receptors; TNFa, tumor necrosis factor alpha; UCP2, uncoupling protein 2.

(Table 1), monocyte chemoattractant protein-1 (MCP-1)
and TNF-a [11,13].
The metabolites (SCFAs) produced in the colon can
stimulate free fatty acid receptor (FFAR 2/3) located on
enteroendocrine L-cells in the colon (Fig. 4), which will
release the anorexigenic gut hormones, for example,
glucagon-like peptide (GLP)-1 and peptide tyrosine
tyrosine (PYY) [11,12]. Canfora and Blaak in 2017
reported that the acetate binds and activates the GPR-
enriched cell and other ligand receptors that inhibit the
secretion of ghrelin. This results in less feeling of hunger
[23,24]. Oral administration of acetate in HFD mice,
SCFA have been shown to decrease the expression of
peroxisome proliferator-activated receptor gamma
(PPARg) in intestinal epithelial organoids and this leads
to increased expression of mitochondrial uncoupling
protein 2 and increased AMP-to-ATP ratio via AMPK
signaling pathway. Consequently, this provides a route to
an increase in energy expenditure, a change from lipid
synthesis to lipid oxidation [11].
Roles of Akkermansia muciniphila in
nonalcoholic fatty liver disease
Multiple studies had been done regarding intestinal
dysbiosis relationships with various diseases, such as
obesity, diabetes, liver diseases and ulcerative colitis.
There are various causes for hepatic disorders, such as
fatty liver disease, chronic alcohol intake and viral
infections [25]. Prolong HFD intake induces dysbiosis,
which leads to invasion of bacterial products from gut into
systemic circulation and transported to the liver [30]. The
bacterial products stimulate lipogenesis and inflammatory
response, which results in nonalcoholic fatty liver disease
(NAFLD) [26,27]. A study conducted in 2013, reported
alteration in microbial population of gut with consump-
tion of HFD, which further leads to hyperglycemia and
fatty liver [33]. The study conducted by Spencer et al. in
2013 reported that HFD is also linked to fatty liver disease
[28]. TLR activation is the frontline in host immune
defense as it stimulates production of pro-inflammatory
cytokines and chemokines against invading pathogens.
However, prolong TLR stimulation may cause harm to
the host [29,30]. TLRs are among the PRRs, which
recognize bacterial and viral components [31]. This
higher expression of TLRs is mainly associated with
NAFLD [15,32]. TLR4 is the well known receptor for
LPS (cell wall component of Gram-negative) bacteria.
Liver has high tolerance to TLR activation and signaling
[39]. This is because symbiont microbiota is able to
inhibit this inflammatory response by interfering in TLR-
dependent nuclear factor kappa B (NF-kB) transcription
[33,34]. TLR signaling is suppressed in the normal liver.
However, pathogenic condition of liver lowers liver

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6 Reviews and Research in Medical Microbiology 2022, Vol 33 No 00

Fig. 4. The Akkermansia muciniphila degradation of mucin and indigestible diet components in short-chain fatty acids activates
various metabolic pathways. This organism is determined to interact directly with several lipid metabolic substances, including
changing the endotoxin level, short-chain fatty acid production and increased fatty acid oxidation. The molecular mechanism of
AKM on host metabolism is represented. AKM, Akkermansia muciniphila; SCFA, short chain fatty acids.

tolerance because of disruption of gut microbiota Role of Akkermansia muciniphila in future

composition, increases TLR expressions (Table 1) [35].
Therefore, we can conclude that dysbiosis induce
metabolic and inflammatory responses play a major role
in pathogenesis of NAFLD.
Gut microbes and TLRs are potential targets in the
treatment of NAFLD. Kim and co-workers in 2020
investigated that AKM-treated mice have more beneficial
gut microbiota compared with non-AKM-treated mice.
AKM improves gut diversity and gut homeostasis [5,36].
AKM treatment reduces invasion and translocation of
pathogenic bacteria by increasing gut microbiota diversity
and strengthening gut barriers. This mechanism reduces
bacterial components in circulation and prevents activa-
tion of hepatic TLRs. This suppresses possible pro-
inflammatory component production, down-regulates
lipogenesis and further prevents the development of
NAFLD [16].
with medical and dietary intervention
Probiotics are live beneficial bacteria that are naturally
produced by the fermentation process in foods like
yogurt, kimchi, and others. The most common probiotic
found in yogurt and fermented products is Lactobacillus
followed by Bifidobacterium. Prebiotic fibers are the
nondigestible part of foods like bananas, garlic, onion,
apples skin, beans, asparagus and many others that enter
the small intestine in an undigested form and are only
fermented in the large colon. This fermentation process
feeds beneficial bacteria in order to increase its number in
our gut for better health and to reduce disease risk.
AKM can be used as a probiotic (Fig. 2) when consumed
in various forms. The abundance of A. muciniphila in the
human gut can be promoted by dietary intervention and
beneficial interaction with drugs. Many research has been

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Akkermansia muciniphila provides benefits to the human gut Tiwari 7

AKM, pasteurized AKM (70 0C, 30 min) exerts more

effects on HFD-induced obesity, glucose tolerance and
insulin resistance. Treatment with the pasteurized AKM
aids in reducing adipocyte diameter and enhances the
number of intestinal goblet cells [51,52].

Apart from dietary intervention, some drugs have been

Fig. 5. Summarized flow sheet of Akkermansia muciniphila
supplements in overweight and obese human volunteers
[21].
done to prove the increase of A. muciniphila abundance
level in association with calorie restriction and consump-
tion of dietary products containing polyphenol (cranber-
ries extract, black tea or red wine grape) and
fructooligosaccharides (FOS) (soybeans, asparagus, shal-
lots and red onions). Dietary polyphenol are natural
antioxidants that elevate A. muciniphila level by protecting
against attacks of free oxygen radicals [37,38].
Roopchand and co-workers found in their research study
that dietary supplementation of cranberry extract and
grape polyphenol increased A. muciniphila abundance in
HFD mice faeces [39,40]. Everard and co-workers found
out that significantly increased abundance A. muciniphila
upon FOS administration for 5 weeks in ob/ob mice
[41–43]. Dao and co-workers reported in their research
that an increase of A. muciniphila was observed in the
lower abundance group after 12 weeks of calorie
restriction period along with an improvement in total
and low-density lipoprotein (LDL) cholesterol levels as
well as waist circumference [44,45].
proven to promote the abundance of AKM in the human
gut. For instance, discoveries have shown that metformin
significantly increases the population of AKM up to 20%
of the bacterial population, which was correlated with its
ability to improve glucose tolerance [53,54]. AKM
produces SCFA, such as acetic acid from mucin and
numerously supplies vitality to goblet cells that produce
mucin, which contributes to an anti-inflammatory
impact and antidiabetic activity. Thus, AKM-positive
interaction with metformin has resulted in enhanced
glucose tolerance [55,56]. Therefore, this organism has
shown tremendous potential to be used as a supplement in
the treatment of metabolic diseases [57,58].
Becken et al. [59] in 2021 categorized all strains of AKM
(Fig. 6) and divided into four phylogroups by 16S rRNA
sequencing to get complete details and gene expression.
The pangenome of AKM strains contain 4982 gene
clusters (Fig. 7). The significant findings of their work
were interpreted pointwise and mentioned that the strains
of all members of AKM-II and AKM-IV phylogroups.
(1) Contains distinct capsule and exopolysaccharide genes.
(2) Contains putative capsular polysaccharide (CPS)
biosynthesis protein EPsC and Epsl.
(3) Contains CMP-N-acetyl neuraminic acid synthetase.
(4) Contains capsule-modifying enzyme.
(5) Contains polysaccharide pyruvyl transferase WcaK.

The unique characteristics and promising outcome by

dietary intervention makes this organism more profound
as an upcoming supplement in the medical field. Earlier
this organism was thought to be pathogenic because of its
process of adhesion and degradation of intestinal mucus
layer [46,47]. However, this organism restricts itself only
up to the outer mucosal layer preventing it from reaching
the inner layer during mucin degradation [48]. Therefore,
this organism is not pathogenic, in fact it prevents
colonization of pathogens because of its strong attach- Fig. 6. Sample collection, factors and results of pediatric
ment to the mucus layer [49,50]. In comparison with live obesity microbiome and metabolome study [50].

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8 Reviews and Research in Medical Microbiology 2022, Vol 33 No 00
Fig. 7. Akkermansia muciniphila pangenome, phylogroups
categories, gene clusters and significant findings in latest
study [50].
(6) Contains Cps locus and two conserved additional loci
then AKM-I.
(7) Phylogroup AKM-IV codes DltB, an enzyme typically
involved in modification of lipoteichoic acid in Gram-
positive bacteria and also modify lipopolysaccharides in
some Gram-negative bacteria.
(8) AKM-I contains additional chemotaxis genes, cyto-
chrome C biosynthetic genes and code for quality
control sensor protein for outer membrane
biogenesis NlpE.
(9) All phylogroups contains FeOAB genes, AKM-I and
AKM-II encoded additional mechanisms, such as
AKM-I contains multiple enterochelin transporter
gene groups, use siderophores to scavenge ferric iron.
AKM-II contains distinct gene groups for ferric iron
transporters than AKM-I. AKM-IV phylogroup lacks
in canonical mechanisms for ferric iron acquisition.
(10) AKM-I and AKM-II phylogroups contains LexA
repressor, indicates an SOS system for differences in
oxygen sensitivity.
(11) All phylogroups encode 27 glycoside hydrolase
enzyme families but varied in abundance of GH
families. AKM-IV phylogroup does not contain GH
97 enzymes, which constitute glycoamylases, such as
Bacteroides thetaiotaomicron Sus B. AKM-IV phy-
logroup also had fewer GH 110 enzymes, which is a
galactosidases enzyme group capable of cleaving blood
group B antigens. Moreover, strains of AKM-IV
phylogroup were enriched for GH 29 and GH 95 L-
fucosidases, responsible for cleaving the terminal
fucose residues that decorate mucin and human
milk oligosaccharides.
(12) Phylogroups AKM-II and AKM-IV are deficient for
reductive sulfur assimilation.
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Conclusion
A. muciniphila is a bacterium that does wonders in the
human body through its abilities to modulate the
intestinal permeability, gut barrier and inflammatory
response. This organism can benefit patients with
diabetes, obesity and NAFLD. In a nutshell, this organism
can be a key role player to fight against diabetes and
obesity. However, further studies should be done to
determine the effects of A. muciniphila in vivo as well as its
safety in humans, probably in upcoming future encoding
genes of AKM could be tailored by latest technologies,
such as CRISPR/cas system to obtain target-based
outcome in patients with metabolic disorders, T2DM
and obesity.
Acknowledgements
Conflicts of interest
There are no conflicts of interest.
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