| mice deficient for SIRT6 are small and at 2-3 weeks of age develop abnormalities that include profound lymphopenia, loss of subcutaneous fat, lordokyphosis, and severe metabolic defects, eventually dying at about 4 weeks and exhibit genome instability ( | |
SIRT6-deficient mice develop normally but succumb to a lethal hypoglycemia early in life ( |
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SIRT6-deficient cells exhibit increased Hif1alpha activity and show increased glucose uptake with upregulation of glycolysis and diminished mitochondrial respiration ( |
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Abrogation of these SIRT6 activities leads to impaired resolution of DNA double-strand break ( |
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liver-specific deletion of SIRT6 in mice causes profound alterations in gene expression, leading to increased glycolysis, triglyceride synthesis, reduced beta oxidation, and fatty liver formation |
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mice overexpressing Sirt6 are protected against diet-induced obesity |
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SIRT6(-/-) animals had very low levels of blood glucose and died shortly after weaning |
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SIRT6-deficient mice have a striking degenerative phenotype leading to shortened lifespan and are associated with hypoglycemia and defects in DNA repair |