When translation meets metabolism: Multiple links to diabetes

Yuguang Shi, Simeon I. Taylor, Seng Lai Tan, Nahum Sonenberg

Research output: Contribution to journalReview article

68 Scopus citations

Abstract

Type 2 diabetes is a polygenic disorder characterized by multiple biochemical defects including transcriptional, translational, and posttranslational abnormalities. Although major progress has been made in elucidation of factors at the transcriptional and posttranslational levels, defects at the translational level remain elusive. Mutation of a kinase that regulates translation initiation has been implicated in the etiology of a monogenic form of diabetes known as Wolcott-Rallison syndrome. Characterization of mice rendered deficient in eukaryotic initiation factors has provided model systems to study the involvement of translation in regulating insulin synthesis and secretion, hepatic function, peripheral insulin resistance, and diabetic complications. Recent progress in the understanding of endoplasmic reticulum overload by unfolded proteins has begun to uncover mechanisms leading to pancreatic β-cell exhaustion. Future advances in this area may lead to identification of the missing links in the pathogenesis of β-cell failures due to conditions such as hyperinsulinemia, hyperglycemia, and long-term treatment with sulfonylureas, and thus may identify novel therapeutic targets for diabetes.

Original languageEnglish (US)
Pages (from-to)91-101
Number of pages11
JournalEndocrine Reviews
Volume24
Issue number1
DOIs
StatePublished - Feb 2003
Externally publishedYes

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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