PRESENTATION
Influence of Probiotics Administration on Gut
Microbiota Core
A Review on the Effects on Appetite Control, Glucose,
and Lipid Metabolism
Silvia Falcinelli, PhD,* Ana Rodiles, PhD,† Azadeh Hatef, PhD,‡
Simona Picchietti, PhD,§ Lina Cossignani, PhD,∥ Daniel L. Merrifield, PhD,†
Suraj Unniappan, PhD,‡ and Oliana Carnevali, PhD*
Abstract: An increasing number of studies has shown that dietary
probiotics exert beneficial health effects in both humans and animals. It
is well established that gut microbiota play a pivotal role in regulating
host metabolism, and a growing number of studies has elucidated that
probiotics positively interfere with gut microbiota. Accumulating evi-
dence shows that probiotics, through their metabolic activity, produce
metabolites that in turn contribute to positively affect host physiology.
For these reasons, probiotics have shown significant potential as a
therapeutic tool for a diversity of diseases, but the mechanisms through
which probiotics act has not been fully elucidated yet. The goal of this
review was to provide evidence on the effects of probiotics on gut
microbiota changes associated with host metabolic variations, specifi-
cally focusing on feed intake and lipid and glucose metabolism. In
addition, we review probiotic interaction with the gut microbiota. The
information collected here will give further insight into the effects of
probiotics on the gut microbiota and their action on metabolite release,
energy metabolism, and appetite. This information will help to improve
knowledge to find better probiotic therapeutic strategies for obesity and
eating disorders.
Key Words: probiotics, lipid metabolism, glucose metabolism,
appetite control, gut microbiota, gut metabolites
(J Clin Gastroenterol 2018;00:000–000)
From the *Department of Life and Environmental Sciences (DiSVA),
Marche Polytechnic University, Ancona; §Department for Innova-
tion in Biological, Agro-food and Forest Systems (DIBAF), Uni-
versity of Tuscia, Viterbo; ∥Department of Economics-Estimative
Science and Food, Bromatological Chemistry Division, Bio-
chemistry, Physiology and Nutrition, University of Perugia, Perugia,
Italy; †Aquatic Animal Nutrition and Health Research Group,
School of Biological Sciences, Plymouth University, UK; and
‡Laboratory of Integrative Neuroendocrinology, Department of
Veterinary Biomedical Sciences, Western College of Veterinary
Medicine, University of Saskatchewan, Saskatoon, Saskatchewan,
Canada.
Supported by FA 2013, PRIN 2010-2011 prot 2010W87LBJ, EU COST
AQUAGAMETS 2012 given to O.C. In addition, this research was
partially funded by a Discovery Grant and Discovery Accelerator
Supplement Award to S.U. Infrastructure for the work conducted in
the laboratory of S.U. was provided by the Canada Foundation for
Innovation—John Evans Leadership Fund and the Saskatchewan
Health Research Foundation (SHRF) Establishment Grant. S.U.
received a Canadian Institutes of Health Research (CIHR) New
Investigator Award. A.H. is a recipient of postdoctoral fellowships
from the CIHR and SHRF.
The authors declare that they have nothing to disclose.
Address correspondence to: Oliana Carnevali, PhD, Department of Life
and Environmental Sciences (DiSVA), Marche Polytechnic Uni-
versity, Brecce Bianche 1 Street, Ancona 60131, Italy
(e-mail: o.carnevali@univpm.it).
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
DOI: 10.1097/MCG.0000000000001064
J Clin Gastroenterol  Volume 00, Number 00, ’’ 2018
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This paper can be cited using the date of access and the unique DOI number which can be found in the footnotes.
he term “probiotic” is derived from the Greek language
T meaning “for life.”
The most commonly used bacteria in probiotics are
mainly members of the genera Lactobacillus and Bifido-
bacterium, and a growing number of strain bacteria are
gaining the role of probiotics.1–3
In the last decades, several studies focused their
attention on the effects of probiotics on the host, showing
that probiotics (eg, Lactobacilli and Bifidobacteria) play the
following roles:
 are able to positively shift gut microbiota balance toward
health-promoting bacteria,4,5
 reinforce gut epithelium architecture by increasing micro-
villi and enterocyte lengths,6–8
 prevent gut inflammation and other intestinal or systemic
disease (ie, inflammatory bowel disease).9–11
In addition, numerous studies, both in animals and
humans, have provided clear evidence that probiotics exert
an improvement on immune response, and promote calci-
fication and growth.12–15
Furthermore, probiotics, through their metabolic
activity, produce several types of metabolites (each probiotic
strain has a specific metabolite profile), such as short-chain
fatty acids (SCFAs), including acetic, butyric, propionic,
and lactic acids.16,17 Recent metabolomic studies found that
the Lactobacillus strain principally produces lactic and
acetic acid, organic acids, and other potentially anti-
microbial metabolites as a product of its metabolic activity.
For example, Lactobacillus plantarum synthesize para-ami-
nobenzoate, an intermediate of folic acid, while Lactoba-
cillus rhamnosus L60 and Lactobacillus fermentum L23 are
producers of bacteriocins.18,19
For the above-mentioned reasons, in the last decade,
probiotics gained popularity both in human medicine and in
aquaculture. In fact, while probiotics are used in humans as
attenuators of intestinal and/or metabolic comorbidities, in
aquaculture, probiotics are used to increase tolerance to
stress, improve the digestibility of nutrients, and promote
reproduction.
In 1857, Louis Pasteur started to study lactic acid fermen-
tation, and about 15 years later, Joseph Lister obtained the first
pure culture of lactic acid bacteria (LAB) (Bacterium lactis).20
LABs are gram-positive, nonsporing, catalase-negative, aero and
acid–tolerant bacteria, and produce several antimicrobial sub-
stances such as lactic acid, which is a major metabolic end-
product of carbohydrate fermentation.20
www.jcge.com |1
Falcinelli et al
LABs include genera including Lactobacillus, Strepto-
coccus, Pediococcus, Lactococcus, and Leuconostoc.21
THE GUT MICROBIOTA AS A “SECOND BRAIN”
The gut microbiota represent a symbiotic association of
a huge number of different bacteria that harbors in the
gastrointestinal tract of all organisms.22
The composition of an individual’s gut microbiota is
unique. The gut microbiota evolves with the host from birth
and develops a mutualistic relation that depends on host
nutrition and individual lifestyle.10,23
The overall balance in the composition of gut microbial
communities is extremely important for ensuring homeo-
stasis of intestinal mucosa.24 Moreover, the symbiotic effects
among bacteria lead to the production of several metabolites
that can influence the host physiology.25,26
Fluctuations in the structure of gut microbial com-
munities, also identified as dysbiosis, may alter positive
interaction among bacteria and their host.27 Consequently,
such changes in the gut microbiota composition and func-
tion may concur with disease susceptibility by altering sev-
eral biochemical functions.27
Because of meta-omics approaches such as meta-
genomics and metabolomics, it is possible to clearly classify
gut microbiota species that inhabit the gut and identify the
metabolites they have produced.23
Indeed, metabolite profiles related to the gut microbiota
can suggest deep insights into the impact of lifestyle and dietary
factors that could lead to specific disease conditions.28
As it is well established that the gut microbiota inter-
acts with the host metabolism and affects physiological or
pathologic conditions, study on its composition helps dis-
criminate between unhealthy and healthy subjects.29
The gut microbiota plays a central role in maintaining
the integrity of the intestinal tract and in regulating multiple
host metabolic pathways.
Furthermore, several reports highlighted the ability of
the gut microbiota to interact with the host’s tissue, con-
trolling its energy metabolism, contributing to variations in
body weight, fat distribution, insulin sensitivity, and lipid
metabolism.30–32
Because of these extraordinary interconnections, gut
microbiota is defined as a “second brain.”33
Communication between the brain and gut is bidirec-
tional, whereby shared signals between the 2 organ systems
are exchanged to coordinate physiological functions.34
Indeed, the gut-brain crosstalk is a complex commu-
nication system that provides to guarantee the correct gas-
trointestinal and central nervous system homeostasis. These
complex connections are included in the denomination of
“gut-brain axis” (GBA).35
Despite the fact that the mechanisms of this commu-
nication are not fully elucidated, such interactions include
neural, humoral, immune, and metabolic pathways.36
Several approaches have been used to better under-
stand the axis communication, such as the use of germ-free
animals or animals exposed to pathogenic bacterial infec-
tion, prebiotics and probiotics, or antibiotics. Results give
arise to the belief that it is clear that the gut microbiota plays
a pivotal role in the regulation of mood, cognition, pain,
and obesity and has a prevailing influence on signaling
besides the GBA.37
Diet is one of the most prominent influencing factors of
the GBA.37
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J Clin Gastroenterol  Volume 00, Number 00, ’’ 2018
There is a pressing need in understanding gut micro-
biota-brain interactions as they may give new insights into
individual alterations in mood, cognition, sleep, eating
behavior, and metabolic pathways.38
Therefore, probiotics can be used to positively alter gut
microbiota, and their ability to improve metabolism is of
interest to many researchers. Indeed, several studies have
highlighted their positive impact on gut microbiota, thus
reflecting an amelioration on host physiology.39,40
In the next section, we will describe the most reliable
mechanisms by which probiotics interact with gut micro-
biota, influences host metabolism and energy storage, and
increases susceptibility to obesity. The interaction of pro-
biotics and how they affect the metabolic status is not
entirely understood yet.
How Probiotics Interact With Gut Microbiota?
The mechanisms by which probiotics interact with gut
microbiota and accomplish their associated health benefits
could have many facets.
Gut microbiota of both humans and animals delivers
an unrestricted number of bioactive substances that can
affect health.41
Despite the fact that mechanisms of probiotics’ action
are still the object of study, several hypotheses have been
proposed.
Probiotics, by interacting with gut microbiota, are able
to produce metabolic compounds, antimicrobial agents, and
health-promoting factors that overwhelm the development
of other bacteria.18,41
In addition, probiotics are able to settle in the gut and
they ferment indigestible carbohydrate deriving from food.42
Their metabolic activity increases the amount of metabolites,
such as SCFAs in the gut, which are produced mainly from
carbohydrates, protein, and peptide.42 SCFAs represent the
final product of bacterial activity in the gastrointestinal tract;
they are able to block the synthesis of hepatic cholesterol,
thus leading to a decrease of lipid amount in the blood.43,44
Furthermore, it has been proposed that probiotics
assimilate cholesterol and use it as reinforcement for their
cell membrane.45
Moreover, it has been suggested that probiotics have
the capability to convert cholesterol into coprostanol, which
is successively eliminated through feces.46
Probiotic are also able to improve the intestinal epithelial
barrier; a study showed that Lactobacilli modulate the tran-
scription of genes encoding adherence junction proteins, such
as E-cadherin and E-catenin in a T84 cell barrier model.
Moreover, it is supposed that increasing the expression of
genes involved in tight junction signaling is a probable mech-
anism to reinforce intestinal epithelial barrier integrity.47
A study performed on germ-free mice inoculated with a
model of human baby microbiota showed that the admin-
istration of Lactobacillus paracasei or L. rhamnosus increased
Bifidobacteria and reduced Clostridium perfringens and
Staphylococcus aureus populations, compared with control
animals.48
A different mechanism proposed for probiotic action is
the adhesion to intestinal mucosa, which represents a
requirement for colonization.49 In addition, adhesion of
probiotics to the intestinal mucosa modulates the immune
system.15
LABs exhibit numerous surface determinants that
interact with intestinal epithelial cells and mucus.50,51
Intestinal epithelial cells secrete a mix of glycoprotein called
J Clin Gastroenterol  Volume 00, Number 00, ’’ 2018 Probiotic Influence on Host’s Energy Balance

mucin, which is the major constituent of mucous, that helps
avoid the adhesion of pathogenic bacteria to the gut.50,51
PROBIOTICS AND LIPID METABOLISM
In the present world scenario, obesity is rapidly
increasing.52 This metabolic disorder gives rise to other
metabolic comorbidities related to glucose metabolism, the
immune system, and appetite.52
Among the several probable factors that lead to the
development of obesity, the role of gut microbiota is very
crucial.27 Indeed, gut microbiota dysbiosis causes dis-
equilibrium in energy homeostasis that finally leads to
obesity.27,28 Several factors have been identified as the key
etiological agents responsible for the progression of obesity,
such as host genetics, metabolism, lifestyle, and diet. How-
ever, the most recent research has highlighted that the gut
microbiota has a dominant role in the onset of obesity and
its relative comorbidities.28
In the last decade, several studies showed that pro-
biotics positively modulate and interact with gut microbiota,
which in turn modify host nutrient metabolism and energy
balance, both in germ-free mice and in zebrafish.8,53,54
As mentioned before, because the number of diseases
associated with lipid metabolism disturbances is increasing
worldwide, several studies have been focused on the ability
of probiotics, mainly Lactobacillus and Bifidobacteria, to
lower lipid profile.45
Hypolipidemic effects of several bacterial strains have
been shown in several animal models (Table 1).
Administration of Lactobacilllus reuteri CRL 1098 at
the concentration of 104 cells/day was able to decrease total
cholesterol and triglyceride content, and showed 17%
increase in the ratio of High-Density Lipoprotein to Low-
Density Lipoprotein, highlighting the effectiveness of the
probiotic in preventing hypercholesterolemia in mice.55
El-Shafie et al56 demonstrated that L. plantarum
NRRL B-4524 used alone or mixed with L. paracasei was
able to lower blood serum cholesterol in rats fed a high-fat
(HF) diet and high-cholesterol diet.
A recent study from our laboratory showed that
administration of L. rhamnosus to adult zebrafish fed a
medium-fat and HF diet (medium-fat diet and HF diet,
respectively) and to 8 dpf zebrafish larvae that receive
commercial feed was able to significantly change gut
microbiota, elevating the abundance of Firmicutes and
reducing the abundance of Actinobacteria. In addition, we
observed that gut microbiota changed by the probiotic was
able to significantly attenuate weight gain, to decrease
transcriptional levels of genes involved in cholesterol (hnf4α
and npc1l1) and triglyceride (fit2 and mgll) metabolism, and,
concomitantly, to lower cholesterol and triglyceride content.
Moreover, we also highlighted changes in SCFA in
zebrafish larvae; in fact, the probiotic increased the amount
of SCFA in the gut. Finally, we observe an amelioration of
gut structure with increased microvilli and enterocyte
height.8,57
In addition, a study performed on HF–fed mice model
showed that supplementation of Bifidobacterium longum and
L. paracasei with fermented ginseng for 9 weeks had an anti-
obese effect, and suppressed weight gain and reduced adi-
pocyte size in the adipose tissue.58
The hypocholesterolemic effects of probiotics has also
been shown in human subjects.
A study highlighted that the probiotic administration
of the Enterococcus faecium M-74 reduces serum cholesterol
concentration by 12% after 56 weeks in 43 volunteers.59
Another study performed on 58 patients showed that
administration of a multistrain probiotic composed by
Lactobacillus+Lactococcus (6×1010 CFU/g), Bifidobacte-
rium (1×1010 CFU/g), Propionibacterium (3×1010 CFU/g),
and Acetobacter (1×106 CFU/g) significantly reduced the
fatty liver index after 8 weeks of supplementation.60
Despite many studies showing significant cholesterol-
lowering effects of probiotics in both animal models and

TABLE 1. Studies on Probiotics and Lipid Profile Performed in Animals and Humans
Dose of the
Probiotic Strain Animal/Human Probiotic Effects References
Lactobacilllus reuteri Mice 4
10 cells/d 17% increase in the ratio of HDL to LDL Taranto et al55
Lactobacillus plantarum Rat 107-8 CFU/g Lower blood serum cholesterol El-Shafie et al56
alone or mixed with
Lactobacillus paracasei
Lactobacillus rhamnosus High-fat–fed 106 CFU/mL Changed gut microbiota and decreased Falcinelli et al57
adult zebrafish triglyceride and cholesterol content
model
L. rhamnosus Zebrafish larvae 106 CFU/mL Increased amount of short-chain fatty acids, Falcinelli et al8
decreased triglycerides and cholesterol content,
increased microvilli and enterocyte heights
Bifidobacterium longum and High-fat–fed 8
5×10 CFU/mL Suppressed weight gain and reduced adipocyte Kang et al58
Lactobacillus paracasei mice model size
Enterococcus faecium Human 2×109 CFU Reduced serum cholesterol concentration by 12% Hlivak et al59
Lactobacillus+Lactococcus, Human 6×1010 CFU/g; Reduced the fatty liver index Kobyliak et al60
Bifidobacterium 1×1010 CFU/g;
Propionibacterium, 3×1010 CFU/g;
Acetobacter 1×106 CFU/g
Lactobacillus fermentum Human 2×109 CFU Did not improve cholesterol profile after 10 d Simons et al61
L. rhamnosus LC 705 and Human 1010 CFU/g Did not decrease cholesterol profile Hatakka et al62
Propionibacterium
freudenreichii ssp
HDL indicates high-density lipoprotein; LDL, low-density lipoprotein.

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Falcinelli et al
humans, it is necessary to take into account that con-
troversial results were obtained.
Another study performed on 46 volunteers aged
between 30 and 75 years of age, showed that administration
of capsules of L. fermentum at the concentration of 2×109
CFU did not improve lipid profile after 10 days of treatment
in patients who had elevated serum cholesterol.61
In addition, in men with a high level of cholesterol, L.
rhamnosus LC 705 and Propionibacterium freudenreichii ssp
shermanii strain JS at 1010 CFU/g did not improve choles-
terol profile.62
PROBIOTICS’ EFFECTS ON GLUCOSE
METABOLISM
In mammals species and teleost fish, glucose metabolism is
controlled by various metabolic pathways.63,64
An alteration of glucose metabolism is connected to a
greater risk of several chronic disorders including diabetes,
dyslipidemia, and obesity. The supplementation of omega-3
fatty acids,65 dairy product,66 and coffee67 can improve the
glycemic profile and prevent diabetes or related comorbidities.
Among several dietary constituents, probiotic benefits
have been deeply investigated for improving glucose profile,
and data from animal models highlighted that probiotics
can reduce blood glucose and insulin resistance.68
The gut hormones such as glucagon-like peptide (GLP)
and peptide YY could affect β-cell function and regulate
energy homeostasis through insulin stimulation and satiety
properties.69
Results from our laboratory showed that admin-
istration of L. rhamnosus 106 CFU/mL to 6 dpf zebrafish
larvae reduced transcript levels of a genes involved in glu-
cose metabolism, such as insulin and glp-1, concomitantly
with a reduction of glucose level, indicating the hypo-
glicemic properties of the probiotic70 (Table 2).
Interestingly, Larsen et al74 showed that humans with
type 2 diabetes (T2D) have altered gut microbiota compared
with nondiabetic counterparts.
In addition, a study on humans performed on 50 vol-
unteers with T2D showed that the consumption of Lacto-
bacillus acidophilus (La-5) and Bifidobacterium animalis
(subsp lactis BB-12) at 109 CFU/day for 6 weeks improved
the glycemic control in T2D subjects by reducing hemo-
globin A1c and fasting plasma glucose.72
Additional studies performed in a HF mice model
reported that Lactobacillus gasseri restored ACSL3-lipid
sensing altered by HF feeding.71
Moreover, a study performed on diet-induced obesity
mice showed that probiotic multistrain administration
TABLE 2. Studies on Probiotics and Glucose Profile Performed in Animals and Humans
Probiotic Strain Animal/Human
Lactobacillus rhamnosus Zebrafish larvae
Lactobacillus gasseri High-fat–fed mice
model
L. rhamnosus, L. acidophilus, and Diet-induced obesity
Bifidobacterium bifidumi mice model
L. acidophilus and Bifidobacterium Type 2 diabetes human
animalis
L. acidophilus and B. animalis Human
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J Clin Gastroenterol  Volume 00, Number 00, ’’ 2018
composed by L. rhamnosus, L. acidophilus, and Bifidobacte-
rium bifidumi at the concentration of 1.8×109 CFU changed
insulin sensitivity.4 However, human clinical study on pro-
biotics and glucose metabolism have shown mixed results.
For instance, another study performed in humans
concluded that the consumption of L. acidophilus (La-5) and
B. animalis (subsp lactis BB-12) at the concentration of
3.0×109 CFU/day did not show benefit on short-term gly-
cemic control.73
EFFECTS OF PROBIOTICS ON APPETITE
CONTROL—AN OVERVIEW ON OREXIGENIC
AND ANOREXIGENIC PEPTIDE REGULATION
In vertebrates, appetite control and energy balance are
regulated by the hypothalamic circuitry, widely conserved
between humans and zebrafish.75,76 A wide network of
molecules regulates appetite control and energy homeo-
stasis, and, among these, leptin is a hormone responsible for
inhibiting food intake and promoting energy expenditure.77
It is well known, through several studies, that mutation in
the ob gene causes leptin deficiency and leads to obesity.78,79
Different studies, both in mammals and fish, showed that
leptin is able to reduce food intake by upregulating anorexi-
genic signals such as melanocortin-4-receptor (MC4R) and
downregulating orexigenic signals such as neuropeptide Y
(NPY) and cannabinoid receptor 1 (CB1).80–82
Knock-out of MC4R directly promoted lipid uptake
and triglyceride synthesis, leading to obesity.83 Fur-
thermore, studies in humans and in mice showed that the
activation of MC4R limits the accumulation of body fat by
reducing food intake.84
In contrast, NPY and its Y receptor stimulate food intake.85
Like NPY, CB1 also is an orexigenic signal responsible
for food intake and weight gain.86 CB1 receptor increases
hepatic lipid accumulation through the stimulation of the
lipogenic transcription factor SREBP-1c and increases de
novo fatty acid synthesis in zebrafish.87
Nowadays, a growing body of evidence supports the
role for gut microbiota in influencing host appetite and food
intake by regulating eating-related behavior.88
Gut microbiota significantly affects the bidirectional
communication between the brain and gastrointestinal tract,
which has been coined as the microbiota-GBA.35,89,90
In addition, supplementation of probiotics modifies gut
microbiota that directly acts on molecules that regulate appetite
and satiety.88
It has been shown the genus Bacteroides is associated
with elevated ingestion of a high-carbohydrate and high-
glycemic index diet91,92 (Table 3).
Dose of the
Probiotic Effects References
106 CFU/mL Reduction of glucose level Falcinelli et al70
109 CFU/ Restores ACSL3-lipid sensing Bauer et al71
0.5 mL
1.8×109 CFU Changed insulin sensitivity Bagarolli et al4
109 CFU/d Improved glycemic control Tonucci et al72
3.0×109 CFU/d Does not show benefit on short-term Ivey et al73
glycemic control
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J Clin Gastroenterol  Volume 00, Number 00, ’’ 2018
TABLE 3. Studies on Probiotics and Appetite Control Performed in Animals
Dose of the
Probiotic Strain Animal/Human Probiotic
Bacteroides — —
Lactobacillus paracasei Pig 1010 CFU/g
Lactobacillus rhamnosus Zebrafish larvae 106 CFU/mL
L. rhamnosus High-fat–fed adult 106 CFU/mL
zebrafish
L. rhamnosus, L. acidophilus, Diet-induced obesity 1.8×109 CFU
and Bifidobacterium bifidumi mice model
Other studies showed the capability of Bifidobacteria to use
host-indigestible carbohydrate complex, which, consequently,
can stimulate their proliferation and metabolic activity.92,94
Overall, there is a growing body of evidence linking the
gut microbiota with appetite; for such reasons, researchers
focus their studies on the manipulation of gut microbiota to
control appetite and the related metabolic comorbidities.
Bjerg et al93 showed that 2 weeks’ administration of L.
paracasei subsp paracasei L. casei W8 (L. casei W8) lowered
food intake in pigs by increasing insulin and GLP-1.
A study from our laboratory showed that admin-
istration of L. rhamnosus at 106 CFU/mL to 6 dpf zebrafish
larvae changed gut microbiota by increasing Firmicutes and
Proteobacteria abundance. In turn, these changes were
associated with a downregulation of orexigenic genes such
as cb1 and npy and upregulation of anorexigenic genes such
as leptin and mc4r concomitantly with a significant reduc-
tion of Artemia salina nauplii intake.70
Another study performed on diet-induced obesity mice
showed that the supplementation of a multistrain probiotic
composed of L. rhamnosus, L. acidophilus, and B. bifidumi at
the concentration of 1.8×109 CFU modulated hypothalamic
control of food intake by improving leptin resistance.4
In addition, administration of L. rhamnosus to adult
zebrafish fed a HF diet was able to change microbiota and
decrease nesfatin-1 peptide concomitantly with an increase
of transcriptional levels of anorexigenic genes such as
nucb2a and glp-1 and decrease of orexigenic gene npy.57
An additional trial performed on 45 obese men and 60
women showed that administration of L. rhamnosus
CGMCC1.3724 at 1.62×108 CFU had a positive effect on
appetite sensations and eating behaviors, as it increased
satiety efficiency.95 Despite a growing number of researchers
focusing on the relationship between gut microbiota, pro-
biotic supplementation, and their relation with appetite
control, this field of research deserves more attention.
CONCLUSIONS
It is well established that the gut microbiota plays a
pivotal role in regulating host metabolism. A growing body
of evidence supports the role of the gut microbiota in
influencing host metabolism and food intake.
Manipulations of the gut microbiota toward those
species which, through the production of metabolites, pos-
itively interact with host physiology may, therefore, provide
a novel approach in the prevention and treatment of meta-
bolic disorders.
In this review, we portrayed the most studied mecha-
nisms through which probiotics act and interact with the
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This paper can be cited using the date of access and the unique DOI number which can be found in the footnotes.
Probiotic Influence on Host’s Energy Balance
Effects References
Associated with elevated ingestion of Wu et al91
a high-carbohydrate diet
Lowered food intake in pigs by increasing Bjerg et al93
insulin and glucagon-like peptide-1
Increased Firmicutes and Proteobacteria and Falcinelli et al70
reduction of Artemia salina nauplii intake
Changed microbiota and decreased nesfatin-1 Falcinelli et al57
peptide
Improved leptin resistance Bagarolli et al4
host. In addition, we reported the most recent evidences of
the action of probiotics on host lipid and glucose metabo-
lism and food intake.
Together, this contributes to better understand the
action of probiotics on gut microbiota, metabolite produc-
tion, and with energy metabolism and appetite. It will,
therefore, contribute to help the selection of probiotics as a
therapeutic tool for metabolic and eating disorders.
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