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The Critical Medical Issue of Type 2 Diabetes Mellitus

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Type 2 Diabetes Mellitus (T2DM)
Diabetes is one the most critical medical issues of our time. According to the Center of Disease Control and Prevention nearly 26 million Americans (approximately 8% of all Americans) have diabetes and an estimated of 79 million adults are pre-diabetes. Approximately $200 billion per year is lost due to diabetes because of medical treatments and lost wages. Insulin resistance and the dysfunction of beta cells are the two pathogenic hallmarks of the development and progression of T2DM. Studies have shown that pancreatic beta cell functional mass is affected in T2DM (1, 2). Secretion of insulin stimulated by glucose is lower in human islets of Langerhans isolated from patients with T2DM than from normal individuals (1, 3). Knowledge of the molecular mechanism underlying defects in beta cell function found in humans and animal models of T2DM is incomplete. Without a more complete understanding of the mechanisms that regulate beta cell insulin secretion we will be unable to develop new approaches to prevent and treat diabetes.

Physiological aspects of beta cell function Beta cells of the endocrine pancreas constantly monitor glucose levels circulating in the blood and respond accordingly by releasing insulin. Glucose is the primary physiological stimulus of insulin secretion. When blood glucose concentration is elevated, glucose is transported across the beta cell plasma membrane by passive diffusion through glucose transporters (GLUT-1

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