Cited by 295Gut microbiota and healthRegulation of Appetite and ObesityGastrointestinal motility and disorders

The DOI matches its Crossref record; 238 of the 238 references it cites were found in a registry or an index.

From gut microbiota to host appetite: gut microbiota-derived metabolites as key regulators

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Abstract

Feelings of hunger and satiety are the key determinants for maintaining the life of humans and animals. Disturbed appetite control may disrupt the metabolic health of the host and cause various metabolic disorders. A variety of factors have been implicated in appetite control, including gut microbiota, which develop the intricate interactions to manipulate the metabolic requirements and hedonic feelings. Gut microbial metabolites and components act as appetite-related signaling molecules to regulate appetite-related hormone secretion and the immune system, or act directly on hypothalamic neurons. Herein, we summarize the effects of gut microbiota on host appetite and consider the potential molecular mechanisms. Furthermore, we propose that the manipulation of gut microbiota represents a clinical therapeutic potential for lessening the development and consequence of appetite-related disorders.

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Crossref · 10.1186/s40168-021-01093-y

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Fig. 1 Gut microbiota-associated mechanisms involved in host appetite control. Firstly, gut microbial metabolites can stimulate enteroendocrine cells to release anorexigenic hormones (PYY, GLP-1, and CCK) and neurotransmitter (5-HT) and promote the secretion of peripheral hormones (leptin, ghrelin, and insulin). Secondly, Igs are involved in modulating the biological activity of appetite-regulating hormones, such as leptin and ghrelin. In addition, gut microbiota can produce identical protein sequences with appetite-regulating peptides, such as ClpB, that might directly act on anorexigenic neurons or bind to Igs to modulate the secretion of anorexigenic hormones from enteroendocrine L cells
Fig. 1 Gut microbiota-associated mechanisms involved in host appetite control. Firstly, gut microbial metabolites can stimulate enteroendocrine cells to release anorexigenic hormones (PYY, GLP-1, and CCK) and neurotransmitter (5-HT) and promote the secretion of peripheral hormones (leptin, ghrelin, and insulin). Secondly, Igs are involved in modulating the biological activity of appetite-regulating hormones, such as leptin and ghrelin. In addition, gut microbiota can produce identical protein sequences with appetite-regulating peptides, such as ClpB, that might directly act on anorexigenic neurons or bind to Igs to modulate the secretion of anorexigenic hormones from enteroendocrine L cellsCC BY · PubMed Central
Fig. 2 Gut microbial metabolites derived from amino acids influence host appetite control. Microbiota-derived amino acids mediate a variety of effects on appetite control. (1) Trp can be metabolized by commensal bacteria to produce tryptamine that affect the production and secretion of 5-HT, and some indole derivatives that are associated with maintaining intestinal permeability. 5-HT can act as neurotransmitter that conveys signals from the gut to the brain and mediate appetite control. (2) Glu can be metabolized by gut microbiota to produce GABA, which is considered a neurotransmitter to regulate the secretion of appetite-related hormones and intestinal motility. (3) Gut microbiota are involved in the biosynthesis and transport of BCAAs. The imbalance of BCAAs: non-BCAAs ratio can influence the 5-HT production in the hypothalamus. In addition, BCAAs can control appetite through mediating intestinal amino acid receptors and hypothalamic NCG2/eIF2α signaling. The sensory, hormonal, and neural signals are sent to the brain through vagal afferents or bloodstream to regulate appetite
Fig. 2 Gut microbial metabolites derived from amino acids influence host appetite control. Microbiota-derived amino acids mediate a variety of effects on appetite control. (1) Trp can be metabolized by commensal bacteria to produce tryptamine that affect the production and secretion of 5-HT, and some indole derivatives that are associated with maintaining intestinal permeability. 5-HT can act as neurotransmitter that conveys signals from the gut to the brain and mediate appetite control. (2) Glu can be metabolized by gut microbiota to produce GABA, which is considered a neurotransmitter to regulate the secretion of appetite-related hormones and intestinal motility. (3) Gut microbiota are involved in the biosynthesis and transport of BCAAs. The imbalance of BCAAs: non-BCAAs ratio can influence the 5-HT production in the hypothalamus. In addition, BCAAs can control appetite through mediating intestinal amino acid receptors and hypothalamic NCG2/eIF2α signaling. The sensory, hormonal, and neural signals are sent to the brain through vagal afferents or bloodstream to regulate appetiteCC BY · PubMed Central
Fig. 3 Potential clinical applications related to gut microbiota in appetite-related disorders. Gut microbial composition and metabolites contribute appetite control through altering the production and secretion of appetite-related hormones and influencing the immune system. Modulation of gut microbial composition is feasible via various strategies, including dietary interventions, probiotics, prebiotics, next-generation probiotics, FMT, and FVT. In addition, postbiotics can specifically and precisely change the microbial metabolites
Fig. 3 Potential clinical applications related to gut microbiota in appetite-related disorders. Gut microbial composition and metabolites contribute appetite control through altering the production and secretion of appetite-related hormones and influencing the immune system. Modulation of gut microbial composition is feasible via various strategies, including dietary interventions, probiotics, prebiotics, next-generation probiotics, FMT, and FVT. In addition, postbiotics can specifically and precisely change the microbial metabolitesCC BY · PubMed Central

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Cites

Research works printed but not linked: 5

  1. Perry RJ, Peng L, Barry NA, Cline GW, Zhang D, Cardone RL, et al. Acetate mediates a microbiome-brain-beta-cell axis to promote metabolic syndrome. Nature. 2016;534:213-7. · DOI · Paper page
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Metadata

Authors
Han, H., Yi, B., Zhong, R., Wang, M., Zhang, S., Ma, J., Yin, Y., Yin, J., Chen, L., & Zhang, H.
Affiliations
  • University of Liège (BE)
  • Chinese Academy of Agricultural Sciences (CN)
  • Hunan Agricultural University (CN)
  • Chinese Academy of Sciences (CN)
Corresponding author
  • Yin, Jie
  • Zhang, Hongfu
Venue
Microbiome
Published
2021-07-20
Volume
9
Issue
1
Pages
162-162
ISSN
2049-2618 (ISSN-L)
OpenAlex
W3184092071
Cited by
292
References
238
Citations by year
2026: 45 · 2025: 67 · 2024: 71 · 2023: 61 · 2022: 41 · 2021: 7
FWCI
4.75
Type
journal article
Language
en
Open access
Locations
  • Microbiome (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • ORBi (University of Liège) (submittedVersion, other-oa)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Natural Science Foundation (31702119, 31672428)
  • Agricultural Science and Technology Innovation Program (CAAS-ZDRW202006-02, ASTIP-IAS07)
  • Central Public-interest Scientific Institution Basal Research Fund, Chinese Academy of Fishery Sciences (Y2021GH01-4)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
Keywords
gut microbiota, appetite regulation, hunger and satiety, microbial metabolites, appetite-regulating hormones, hypothalamic neurons, immune system, metabolic disorders, microbiome manipulation
MeSH terms
Gastrointestinal Microbiome, Animals, Appetite, Appetite Regulation, Humans, Immune System

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