ID'ing a novel inhibitor of β-cell function, Id1
- PMID: 21949000
- PMCID: PMC3178278
- DOI: 10.2337/db11-1084
ID'ing a novel inhibitor of β-cell function, Id1
Comment on
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Expression profiling of palmitate- and oleate-regulated genes provides novel insights into the effects of chronic lipid exposure on pancreatic beta-cell function.Diabetes. 2002 Apr;51(4):977-87. doi: 10.2337/diabetes.51.4.977. Diabetes. 2002. PMID: 11916915
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Chronic hyperglycemia, independent of plasma lipid levels, is sufficient for the loss of beta-cell differentiation and secretory function in the db/db mouse model of diabetes.Diabetes. 2005 Sep;54(9):2755-63. doi: 10.2337/diabetes.54.9.2755. Diabetes. 2005. PMID: 16123366
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Inhibition of Id1 augments insulin secretion and protects against high-fat diet-induced glucose intolerance.Diabetes. 2011 Oct;60(10):2506-14. doi: 10.2337/db11-0083. Epub 2011 Sep 22. Diabetes. 2011. PMID: 21940780 Free PMC article.
References
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- Kjørholt C, Åkerfeldt MC, Biden TJ, Laybutt DR. Chronic hyperglycemia, independent of plasma lipid levels, is sufficient for the loss of beta-cell differentiation and secretory function in the db/db mouse model of diabetes. Diabetes 2005;54:2755–2763 - PubMed
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- Busch AK, Cordery D, Denyer GS, Biden TJ. Expression profiling of palmitate- and oleate-regulated genes provides novel insights into the effects of chronic lipid exposure on pancreatic β-cell function. Diabetes 2002;51:977–987 - PubMed
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- Wice BM, Bernal-Mizrachi E, Permutt MA. Glucose and other insulin secretagogues induce, rather than inhibit, expression of Id-1 and Id-3 in pancreatic islet beta cells. Diabetologia 2001;44:453–463 - PubMed
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