When Translation Meets Metabolism: Multiple Links to Diabetes
Yuguang Shi,
Simeon I. Taylor,
Seng-Lai Tan and
Nahum Sonenberg
Endocrine Research (Y.S., S.I.T.), Infectious Diseases (S.-L.T.), Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana 46285; and Department of Biochemistry and McGill Cancer Center (N.S.), McGill University, Montréal, Quebéc H3G 1Y6, Canada
Correspondence: Address all correspondence and requests for reprints to: Dr. Nahum Sonenberg, Department of Biochemistry, McGill University, McIntyre Medical Services Building, 3655 Drummond Street, Room 807, Montréal, Quebéc H3G 1Y6, Canada. E-mail: nsonen{at}med.mcgill.ca; or to Dr. Yuguang Shi, Endocrine Research DC 0545, Lilly Research Laboratories, Lilly Corporate Center, Eli Lilly and Company, Indianapolis, Indiana 46033. E-mail: shi_yuguang{at}lilly.com
Type 2 diabetes is a polygenic disorder characterized by multiplebiochemical defects including transcriptional, translational,and posttranslational abnormalities. Although major progresshas been made in elucidation of factors at the transcriptionaland posttranslational levels, defects at the translational levelremain elusive. Mutation of a kinase that regulates translationinitiation has been implicated in the etiology of a monogenicform of diabetes known as Wolcott-Rallison syndrome. Characterizationof mice rendered deficient in eukaryotic initiation factorshas provided model systems to study the involvement of translationin regulating insulin synthesis and secretion, hepatic function,peripheral insulin resistance, and diabetic complications. Recentprogress in the understanding of endoplasmic reticulum overloadby unfolded proteins has begun to uncover mechanisms leadingto pancreatic ß-cell exhaustion. Future advances inthis area may lead to identification of the missing links inthe pathogenesis of ß-cell failures due to conditionssuch as hyperinsulinemia, hyperglycemia, and long-term treatmentwith sulfonylureas, and thus may identify novel therapeutictargets for diabetes.
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