**1. Introduction**

Type 2 diabetes mellitus (DM2) is a complex metabolic and endocrine disorder resulting from the interaction between genetic and environmental factors, which cause different degrees of alteration in insulin functionality on peripheral tissues, as well as in the pancreatic β cell. Underlying pathologies such as excess weight and obesity, particularly of the android type, are the main factors that favor the development of DM2 [1, 2].

In absolute terms, insulinemia of diabetic subjects may be similar to those of euglycemic individuals but are proportionally insufficient in the hyperglycemia states. Reduced insulin action, for determined levels of the hormone, is known as insulin resistance (IR). When β cells undergo IR, initially there is insulin hypersecretion which compensates for the lack of hormonal action. Hyperglycemia only manifests when there exists a relative insulin hyposecretion to the glucose stimulus [3].
