Figure 1.

Gut microbiota and energy balance. The gut microbes can benefit the host by extracting energies from otherwise non-digestible carbohydrates and plant polysaccharides via enzymes not encoded by humans. Short-chain fatty acids (SCFAs) modulate intestinal gluconeogenesis via the gut-brain neuronal circuit, involving GPR41 (free fatty acid receptor, FFAR3) and through the cyclic adenosine monophosphate (cAMP)-dependent pathway. Butyrate is able to regulate the appetite in the central nervous system by stimulating the liberation of peptide YY (PYY) and the satietogenic hormone glucagon-like peptide 1 (GLP-1) from enteroendocrine L-cells. PYY decreases the intestinal transit rate and increases the harvest of energy from the diet, while GLP-1 improves adipocyte insulin sensitivity and remarkably reduces fat storage in adipose tissue. Gut microbes can also control the metabolic activity of the host by affecting the composition and the abundance of certain bile acid species. In the ileum microbes deconjugate cholic and chenodeoxycholic acids, which escape intestinal uptake, and are converted into secondary bile acids. Bile acids can also act as signaling molecules by binding cellular receptors such as the bile-acid-synthesis controlling nuclear receptor farnesoid X receptor (FXR), G-protein-coupled receptors (GPCR), and TGR5. While primary bile acids can impair glucose metabolism by binding FXR, secondary bile acids, by binding TGR5, improve glucose homeostasis and increase energy expenditure in skeletal muscle.