The Role of the Gut Microbiome in Energy Balance With a Focus on the Gut-Adipose Tissue Axis

Abstract

Obesity is a complex disease attributable to many factors including genetics and environmental influences. Growing evidence suggests that gut microbiota is a major contributing factor to the pathogenesis of obesity and other metabolic disorders. This article reviews the current understanding of the role of gut microbiota in the regulation of energy balance and the development of obesity, and how the microbiota communicates with host tissues, in particular adipose tissue. We discuss several external factors that interfere with the interplay between gut microbiota and host tissue metabolism, including cold exposure, diet regimens, and genetic manipulations. We also review the role of dietderived metabolites that regulate thermogenesis and thus energy homeostasis. Among the gut microbial metabolites, we emphasize short-chain fatty acids, which could be utilized by the host as a direct energy source while regulating the appetite of the host through the gut-brain axis.

Adipose Tissue and Endocrine-Disrupting Chemicals: Does Sex Matter?

“…Obesity and insulin resistance in humans and rodents are associated with intestinal dysbiosis which is characterized by the enrichment of certain species of bacteria to the detriment of others (e.g., a change in the ratio of Firmicutes and Bacteroidetes which are the two dominant phyla representing more than 90% of the total community) with changes in the composition of the gut microbiota [ 200 , 201 ]. The gut-adipose axis depends on communication through short-chain fatty acids (SCFAs) and bile acids (BAs) which behave as hormone-like products signaling through G protein-coupled receptors (GPRs) expressed in the adipose tissue [ 202 , 203 ]. SCFAs which include acetate, propionate, and butyrate are the major end-products of microbial fermentation of dietary fiber.…”

“…They serve as the primary energy source for colonic epithelium and deficiency in SCFA production is associated with type 2 diabetes. SCFAs communicate with the adipose tissue through GPR43 and GPR41 to promote energy metabolism, insulin sensitivity, glucose tolerance, and adipokine secretion [ 202 , 203 ]. BAs are the end-products of cholesterol which exert among others, metabolically beneficial functions in the adipose tissue through promoting beiging and enhancing thermogenesis upon activation of the bile acid-responsive G-protein-coupled receptor TGR5 [ 204 ].…”

FGF15/19 is required for adipose tissue plasticity in response to thermogenic adaptations

“…Several observations support the idea that there is cross-talk between the intestine and thermogenic activation of adipose tissues. Manipulation of the intestinal microbiota has been reported to influence BAT activity and WAT browning in distinct experimental settings [ 9 , 10 , 11 , 12 ]. The endocrine factor GLP-1 originating in the intestine is known to induce BAT thermogenic activity and browning, mostly through an indirect hypothalamus-mediated mechanism [ 13 ].…”

Adiposity in Depression or Depression in Adiposity? The Role of Immune-Inflammatory-Microbial Overlap

“…Increasing evidence suggests that an aberrant gut microbiota may be bidirectionally connected with disturbances in the HPA axis [62], chronic inflammation [47,63], and OxS exacerbation in tissues [64], as well as dysfunction in BAT and reduction in the browning process of WAT [65,66]. Therefore, it may serve as a link between MetS, depression and dysbiosis.…”