Fatty Acid Escape Hypothesis: The Pathway to Type-2 Diabetes

Abstract

Obesity and Type 2 diabetes mellitus (T2DM) are closely related such that together these are generally called diabesity, the underlying
causes of which revolve around the functioning of insulin. Methods PubMed was searched using the following Mesh [(“Adipocytes/classification”[Mesh] OR “Adipocytes/cytology”[Mesh] OR “Adipocytes/ metabolism”[Mesh] OR “Adipocytes/pathology” [Mesh] OR “Adipocytes/physiology”[Mesh]) OR “Fatty acids (FA)” [Mesh]. Results The interaction of insulin with the whole body systems is extensive and resistance to insulin can occur due to multiple reasons including sepsis, Cushing’s syndrome, or even with pregnancy. In this review of literature, our focus is primarily on insulin resistance that is associated with obesity. Insulin promotes lipogenesis in the liver and promotes glucose uptake by skeletal muscles and adipose tissues. Also, insulin inhibits lipolysis in adipose tissue to allow triacylglycerides (TAG) storage in the anhydrous droplet form. When insulin resistance ensues, the delicate balance will tilt to a self-enabling cycle that culminates in the development of T2DM “Diabesity”. Conclusion This review of literature also discusses the hypothetical cascade of defective expansion of adipose tissue due to fatty acids escape, chronic inflammatory state, and ectopic fat deposition in the omentum, liver and skeletal muscles that underlie the pathogenesis of this disease process.