ABSTRACT

Diabetes mellitus (DM) has emerged as one of the most common diseases of this century. Its incidence is on the rise and the numbers are projected to reach a dreaded level by the year 2030 (1). In the United States alone, 4000 cases of diabetes are diagnosed every day (2). Most of them are type 2 diabetes mellitus (T2DM), and overall 8% of the population carries this diagnosis (3). Hyperglycemia is the sine qua non for diabetes. It results from the disturbance of normal glucose homeostasis. Under normal physiological conditions, plasma glucose concentrations are maintained within a narrow range, despite wide fluctuations in supply and demand, through a tightly regulated and dynamic interaction between tissue sensitivity to insulin and insulin secretion (4). Several pathologic processes can result in the disturbance of this balance. These range from autoimmune destruction of the b-cells of the pancreas with consequent insulin deficiency in T1DM to abnormalities that result in insulin resistance in the majority of T2DM. Impairment of insulin secretion and defects in insulin action frequently coexist in the same patient with T2DM. It is often difficult to decipher which abnormality, if either alone, is the primary cause of hyperglycemia (5).