Intestinal microbiota and type 2 diabetes: from mechanism insights to therapeutic perspective

Abstract

The incidence of type 2 diabetes (T2DM) is rapidly increasing worldwide. However, the pathogenesis of T2DM has not yet been well explained. Recent evidence suggests that the intestinal microbiota composition is associated with obesity and T2DM. In this review, we provide an overview about the mechanisms underlying the role of intestinal microbiota in the pathogenesis of T2DM. There is clear evidence that the intestinal microbiota influences the host through its effect on body weight, bile acid metabolism, proinflammatory activity and insulin resistance, and modulation of gut hormones. Modulating gut microbiota with the use of probiotics, prebiotics, antibiotics, and fecal microbiota transplantation may have benefits for improvement in glucose metabolism and insulin resistance in the host. Further studies are required to increase our understanding of the complex interplay between intestinal microbiota and the host with T2DM. Further studies may be able to boost the development of new effective therapeutic approaches for T2DM.

Keywords: Bile-acid metabolism; Body weight; Insulin resistance; Intestinal microbiota; Intestinal microbiota modulation; Type 2 diabetes.

Figure 1

Influence of the intestinal microbiota in promoting gut permeability and insulin resistance. Changes in the intestinal microbiota reduce tight junction proteins of gut epithelial cells and increase gut permeability, thus promoting metabolic endotoxemia and insulin resistance. LPS: Lipopolysaccharide.

Figure 2

Role of the intestinal microbiota in the pathogenesis of type 2 diabetes. The intestinal microbiota may play an important role in the onset of type 2 diabetes by influencing body weight, bile acid metabolism, proinflammatory activity, NAFLD and insulin resistance, and modulating gut hormones. NAFLD: Non-alcoholic fatty liver disease; SCFAs: Short-chain fatty acids; FXR: Farnesoid X receptor; GLP: Glucagon-like peptide; PYY: Peptide YY.