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- W2112890528 endingPage "101" @default.
- W2112890528 startingPage "91" @default.
- W2112890528 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 beta-cell exhaustion. Future advances in this area may lead to identification of the missing links in the pathogenesis of beta-cell failures due to conditions such as hyperinsulinemia, hyperglycemia, and long-term treatment with sulfonylureas, and thus may identify novel therapeutic targets for diabetes." @default.
- W2112890528 created "2016-06-24" @default.
- W2112890528 creator A5007657047 @default.
- W2112890528 creator A5017441842 @default.
- W2112890528 creator A5019957951 @default.
- W2112890528 creator A5064924632 @default.
- W2112890528 date "2003-02-01" @default.
- W2112890528 modified "2023-10-14" @default.
- W2112890528 title "When Translation Meets Metabolism: Multiple Links to Diabetes" @default.
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