Abstract
Insulin is essential for proper control of the concentration of glucose in the blood, and failure of insulin signaling contributes to type 2 diabetes mellitus. The insulin receptor produces multiple intracellular signals, however, and it has not been clear which of these are important for regulation of metabolism in liver and muscle and thus of blood glucose concentrations. Cho et al. report that animals lacking the protein kinase Akt2 (also known as protein kinase Bβ) were mildly hyperglycemic and that insulin appeared to be less effective in these animals than in wild-type animals in causing glucose uptake from the blood. Insulin's effect to suppress glucose production from the liver was strongly decreased. Thus, signaling through Akt2 appears to account for physiologically relevant metabolic effects of insulin. H. Cho, J. Mu, J. K. Kim, J. L. Thorvaldsen, Q. Chu, E. B. Crenshaw III, K. H. Kaestner, M. S. Bartolomei, G. I. Shulman, M. J. Birnbaum, Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKB). Science 292 , 1728-1731 (2001). [Abstract] [Full Text]
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