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.Euffm8RKdwQpaRBJkQtTtQVideo abstract

Highlights

  • Feelings of hunger and satiety are principal involuntary motivations for feeding behavior in humans and animals [1,2,3,4]

  • In another study using piglets, long-term dietary deficiency of branchedchain amino acids (BCAAs) inhibits food intake which might be associated with the enhanced expression of intestinal amino acid receptors, type-1 taste receptors 1 (T1R1) and type-1 taste receptors T1R3, that can activate the CCK secretion and the enhanced hypothalamic GCN2-Eif2α signaling that is involved in the energy metabolism and inhibiting appetite [168]

  • Ortega-Vega et al found that the gut microbial diversity and some specific gut microbiota with heritability are associated with the variants in these genes encoding ghrelin, Melanocortin-4 receptor (MC4R), GLP-1, neuropeptide tyrosine (NPY), and peptide YY (PYY) and metabolic diseases, revealing that, to some extent, the intricate links between host genetics and gut microbiota are related to appetite modulation, which expands our understanding of the functional attributes of the gut Decreased food intake

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Summary

Introduction

Feelings of hunger and satiety are principal involuntary motivations for feeding behavior in humans and animals [1,2,3,4]. In vivo and in vitro studies showed that the translocation of living gut microbiota to adipose tissues induced by increased intestinal permeability influences energy metabolism through inhibiting the leptin signaling in obese humans and mice [36, 37].

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