Plasma Non-Esterified Fatty Acids (NEFA) in Type 2 Diabetes Mellitus: Evidence on Pathophysiology

Abstract

Type 2 diabetes mellitus (T2DM) is a metabolic dysfunction characterized by elevated levels of blood glucose as well as impaired lipid and protein metabolism [1,2]. The mobilization of fatty acids is augmented in insulin resistance due to the failure of lipolysis inhibition by the hormone that further augments the increase in plasma NEFA levels. This in turn, results in inflammation as well as further insulin resistance [3]. The complementation of insulin resistance with dysfunction of pancreatic islet β-cells leads to hyperglycemia. Insulin resistance may persist unnoticed for several years prior to onset of T2DM. Insulin inhibits lipolysis of stored fat in adipose tissue and gluconeogenesis in liver. It also increases the synthesis of proteins needed for the optimal cellular function, repair, growth, and stimulates the translocation of the GLUT-4 protein leading to increased transport of glucose into the muscle cells [4]. Insulin resistance is a metabolic dysfunction that is often mediated by increased inflammation.