【摘 要】
：
Mammalian Sirtl, the closest homolog of yeast sir2, is a NAD+ dependent protein deacetylase.Liver specific deletion of Sirtl abolished AKT activation upon i
【机 构】
：
The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK),National Institute of H
【出 处】
：
2014 International Conference on Aging and Disease(2014年第一届衰
论文部分内容阅读
Mammalian Sirtl, the closest homolog of yeast sir2, is a NAD+ dependent protein deacetylase.Liver specific deletion of Sirtl abolished AKT activation upon insulin stimulation;leads to hepatic hyperglycemia, fatty liver and eventually type 2 diabetes.Pancreatic deletion of Sirt1 impaired beta-cell formation;results in hyperglycemia as well.In combination with p53, whole body Sirt1 haplo-efficiency displayed carcinoma in mammary gland, endothelial compartment and lymphoma.At last, loss of SIRT1 disrupts circadian clock, and leads to premature aging phenotype.With above evidence, we predict utilization ofSirt1 angonists might generate clinical benefits.
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