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Increased Insulin Translation from an Insulin Splice-Variant Overexpressed in Diabetes, Obesity, and
 

Summary: Increased Insulin Translation from an Insulin Splice-
Variant Overexpressed in Diabetes, Obesity, and
Insulin Resistance
Alexandra H. Minn, Hong Lan, Mary E. Rabaglia, David M. Harlan, Brenda A. Peculis, Alan D. Attie,
and Anath Shalev
Department of Medicine, University of Wisconsin (A.H.M., A.S.), Madison, Wisconsin 53792;
Department of Biochemistry, University of Wisconsin (H.L., M.E.R., A.D.A.), Madison, Wisconsin
53706; and National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of
Health, Department of Health and Human Services (D.M.H., B.A.P.), Bethesda, Maryland 20892
Type 2 diabetes occurs when pancreatic -cells
become unable to compensate for the underlying
insulin resistance. Insulin secretion requires -cell
insulin stores to be replenished by insulin biosyn-
thesis, which is mainly regulated at the transla-
tional level. Such translational regulation often in-
volves the 5 -untranslated region. Recently, we
identified a human insulin splice-variant (SPV) al-
tering only the 5 -untranslated region and confer-
ring increased translation efficiency. We now de-
scribe a mouse SPV (mSPV) that is found in the

  

Source: Attie, Alan D. - Department of Biochemistry, University of Wisconsin at Madison

 

Collections: Biology and Medicine