A review of the existing views is given, focused on the role of insulin resistance (IR), impaired insulin secretion and reduced suppression of hepatic glucose output and in the pathogenesis of noninsulin dependent diabetes mellitus (NIDDM). Currently, there are two basic theories on the sequence of these defects. Most of the authors suggest that NIDDM is caused primarily by insulin resistance (IR) (which is also considered an earliest detectable defect) with subsequent inability of the pancreas sufficiently compensate for IR. However, some authors suggest that NIDDM results from the abnormal pancreatic beta-cell function (disturbed pulsatility and first-phase of stimulated insulin secretion). These authors consider IR a secondary defect. It seems, that both these theories are well founded. Actually NIDDM is not a single disorder but is rather a syndrome of diverse etiology and pathogenesis. In case of NIDDM with obesity the primary etiopathogenetic role can be rather ascribed to IR. while in non-obese NIDDM subjects the secretory defect is more probable as a primary cause.

Keywords: Diabetes Mellitus, Type 2 /metabolism/; Glucose /metabolism/; Humans; Insulin /metabolism/; Insulin Resistance /physiology/; Insulin Secretion; Liver /metabolism/