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Type 2 diabetes is a progressive disease in which the risks of myocardial infarction, stroke, microvascular events, and mortality are all strongly associated with hyperglycemia (1). The disease course is primarily characterized by a decline in �-cell function and worsening of insulin resistance. The process is manifested clinically by deteriorations in multiple parameters, including A1C, fasting plasma glucose (FPG), and postprandial glucose levels. In this review, we will evaluate our current understanding of the role played by deteriorating �-cell function and other abnormalities linked with the progression of type 2 diabetes. An improved understanding of these abnormalities may provide the scientific groundwork for novel therapies that may help achieve and maintain good glycemic control.
Vivian Fonseca (Thu,) studied this question.