Modulation of Short-Chain Fatty Acids as Potential Therapy Method for Type 2 Diabetes Mellitus

Figure 1

T2DM pathophysiology. A matrix of negative genetic, epigenetic, and lifestyle factors interact with one another and induce dysfunction of pancreatic β-cells and insulin resistance in the liver, skeletal muscle, or adipose tissue, thereby leading to the development of hyperinsulinemia and hyperglycemia. Moreover, once reduced lipid-buffering capacity in adipose tissue occurs, circulating lipid concentrations increase, leading to ectopic fat storage in the liver, skeletal muscle, and pancreas as well as the development of insulin resistance and dysfunction of pancreatic β-cells. In addition, inflamed adipose tissue results in a low-grade systemic inflammation, which contributes to the development of insulin resistance and T2DM. FFA, free fatty acid; GSIS, glucose-stimulated insulin secretion; T2DM, type 2 diabetes mellitus.