Advances in MRS of Diabetes and Obesity

The pathophysiology of type-2 diabetes implies defects in tissue sensitivity to insulin and in an appropriate insulin secretion. Normally, insulin binds to insulin receptors on target organ cells, resulting in a series of cellular events promoting intracellular glucose transport and metabolism. Insulin resistance is defined by the inability of peripheral target tissue to respond properly to normal concentrations of circulating insulin. This is compensated by the pancreas secreting an increased amount of insulin in order to maintain euglycemia. After this first period of compensated insulin resistance, impaired glucose tolerance develops despite elevated insulin concentrations, and insulin resistance amplifies. Finally, the increased insulin secretion results in a progressive pancreatic β-cell dysfunction leading to decreased insulin secretion. Overt clinical diabetes emerges when these two factors, insulin resistance and impaired β-cell function, occur simultaneously (1). Although not all individuals who are insulin resistant will progress to clinical diabetes, the proportion of patients developing diabetes is high.