The Gut-Brain Axis, the Human Gut Microbiota and Their Integration in the Development of Obesity

Abstract

Obesity is a global epidemic, placing socioeconomic strain on public healthcare systems, especially within the so-called Western countries, such as Australia, United States, United Kingdom, and Canada. Obesity results from an imbalance between energy intake and energy expenditure, where energy intake exceeds expenditure. Current non-invasive treatments lack efficacy in combating obesity, suggesting that obesity is a multi-faceted and more complex disease than previously thought. This has led to an increase in research exploring energy homeostasis and the discovery of a complex bidirectional communication axis referred to as the gut-brain axis. The gut-brain axis is comprised of various neurohumoral components that allow the gut and brain to communicate with each other. Communication occurs within the axis via local, paracrine and/or endocrine mechanisms involving a variety of gut-derived peptides produced from enteroendocrine cells (EECs), including glucagon-like peptide 1 (GLP1), cholecystokinin (CCK), peptide YY3−36 (PYY), pancreatic polypeptide (PP), and oxyntomodulin. Neural networks, such as the enteric nervous system (ENS) and vagus nerve also convey information within the gut-brain axis. Emerging evidence suggests the human gut microbiota, a complex ecosystem residing in the gastrointestinal tract (GIT), may influence weight-gain through several inter-dependent pathways including energy harvesting, short-chain fatty-acids (SCFA) signalling, behaviour modifications, controlling satiety and modulating inflammatory responses within the host. Hence, the gut-brain axis, the microbiota and the link between these elements and the role each plays in either promoting or regulating energy and thereby contributing to obesity will be explored in this review.

Chicory fibre improves reproductive performance of pregnant rats involving in altering intestinal microbiota composition

“…Notably, SCFAs always act on the GPRs, FFAR2 and FFAR3 to induce the release of gut peptides (GLP‐1 and PYY) (Lin et al . 2012; Bliss and Whiteside 2018). Our results also showed that the mRNA expressions of SCFA receptor GPR41 and GPR43 increased, suggesting that SCFAs are greatly utilized by the host.…”

Gut Microbiome, Intestinal Permeability, and Tissue Bacteria in Metabolic Disease: Perpetrators or Bystanders?

“…Connecting pathways include gut hormone signaling to modulate appetite and gut motility, tryptophan metabolism and vagal nerve signaling, as well as SCFA effects on several tissues including adipose tissue to regulate the secretion of cytokines with central regulatory effects. The gut microbiome has moreover been suggested to influence behavior including feeding but also enteric inflammation leading to obesity, all of which have been reviewed in detail elsewhere [187]. The gut microbiome has proven essential for the development of the enteric nervous system by regulation of serotonin production and tryptophan metabolism as well as modulating 5-HT4R-specific signaling.…”

Revisiting the Bacterial Phylum Composition in Metabolic Diseases Focused on Host Energy Metabolism

“…tion of several hormones [46]. These gut microbiota-derived metabolites can modulate the nervous network through afferent nerves and gut hormone secretion including peptide YY (PYY), glucagon like peptide-1 (GLP-1), and cholecystokinin (CCK) [46,47]. The gut microbiota-producing SCFAs can also modulate appetite and food intake via the gut-brain axis.…”