Crosstalk between gut microbiota and antidiabetic drug action

Abstract

Type 2 diabetes (T2D) is a disorder characterized by chronic inflated blood glucose levels (hyperglycemia), at first due to insulin resistance and unregulated insulin secretion but with tendency towards global spreading. The gut microbiota is recognized to have an influence on T2D, although surveys have not formed a clear overview to date. Because of the interactions between gut microbiota and host homeostasis, intestinal bacteria are believed to play a large role in various diseases, including metabolic syndrome, obesity and associated disease. In this review, we highlight the animal and human studies which have elucidated the roles of metformin, α-glucosidase inhibitors, glucagon-like peptide-1 agonists, peroxisome proliferator-activated receptors γ agonists, inhibitors of dipeptidyl peptidase-4, sodium/glucose cotransporter inhibitors, and other less studied medications on gut microbiota. This review is dedicated to one of the most widespread diseases, T2D, and the currently used antidiabetic drugs and most promising new findings. In general, the gut microbiota has been shown to have an influence on host metabolism, food consumption, satiety, glucose homoeostasis, and weight gain. Altered intestinal microbiota composition has been noticed in cardiovascular diseases, colon cancer, rheumatoid arthritis, T2D, and obesity. Therefore, the main effect of antidiabetic drugs is on the microbiome composition, basically increasing the short-chain fatty acids-producing bacteria, responsible for losing weight and suppressing inflammation.

Keywords: Dipeptidyl peptidase-4 inhibitors; Glucagon-like peptide-1 agonists; Gut microbiota; Metformin; Peroxisome proliferator-activated receptors γ agonists; Sodium/glucose cotransporter inhibitors; Type 2 diabetes; α-glucosidase inhibitors.

Figure 1

Crosstalk between metformin action and gut microbiota. GLP1: Glucagon-like peptide-1; GLP2: Glucagon-like peptide-2; LPS: Lipopolysaccharide; SCFA: Short-chain fatty acid.