Possible Mechanisms of Insulin Resistance in Obese Subjects

Abstract

Obesity is characterized by excessive triglyceride accumulation in adipose tissue cells
(adipocytes); the adipocytes are not just a reservoir for storage of energy in the form of triglyceride,
but more importantly act as endocrine cells; they secrete several hormones as leptin and
adiponectin, also secrete adipokines as TNF-α, Interleukin 6 (IL-6) and Plasminogen activator
inhibitor-1 (PAI-1). In obese subjects, adipocytes release high levels of free fatty acids (FFA)
and its metabolites; Diacylglycerol (DAG) and ceramide.1
Acquired insulin resistance is associated with obesity. Insulin resistance is classically
defined as impaired insulin-mediated glucose disposal in skeletal muscle. There are several
mechanisms responsible for insulin resistance in obese subjects, which can be classified into
either to activation of inflammatory pathways or changes in lipoproteins and apoprotein concentrations
as result of associated dyslipidemias.1,2.