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The Cellular Fate of Glucose and Its Relevance in Type 2 Diabetes

Harvard Medical School (C.B., S.S., C.R.K., A.B.G.), Boston, Massachusetts 02115; Joslin Diabetes Center (C.B., S.S., C.R.K., A.B.G.), Boston, Massachusetts 02215; and Beth Israel Deaconess Medical Center (S.S., C.R.K., A.B.G.), Boston, Massachusetts 02215

Correspondence: Address all correspondence and requests for reprints to: Allison B. Goldfine, M.D., Joslin Diabetes Center, One Joslin Place, Boston, Massachusetts 02215. E-mail: allison.goldfine{at}joslin.harvard.edu

Type 2 diabetes is a complex disorder with diminished insulin secretion and insulin action contributing to the hyperglycemia and wide range of metabolic defects that underlie the disease. The contribution of glucose metabolic pathways per se in the pathogenesis of the disease remains unclear. The cellular fate of glucose begins with glucose transport and phosphorylation. Subsequent pathways of glucose utilization include aerobic and anaerobic glycolysis, glycogen formation, and conversion to other intermediates in the hexose phosphate or hexosamine biosynthesis pathways. Abnormalities in each pathway may occur in diabetic subjects; however, it is unclear whether perturbations in these may lead to diabetes or are a consequence of the multiple metabolic abnormalities found in the disease. This review is focused on the cellular fate of glucose and relevance to human type 2 diabetes.

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