Mice homozygous for the Sirt1super BAC are viable and fertile. These mice express a wild-type mouse sirtuin 1 (Sirt1) gene directed by its endogenous promoter/enhancer regions on the BAC transgene. The donating investigator reports that genomic construct also contains the adjacent DnaJ (Hsp40) homolog, subfamily C, member 12 (Dnajc12) gene, but notes the absence of effect of DNAJC12 inhibition on the molecular pathways affected by SIRT1. SIRT1 is a protein deacetylase involved with telomere deacetylation, DNA repair, energy homeostasis. As such SIRT1 plays roles in telomere length maintenance, tumor growth, and improved metabolic syndrome caused by high fat diets. Sirt1super mice exhibit a threefold increase in SIRT1 expression in liver, brown adipose tissue, and muscle. On a high fat diet they show lower lipid induced inflammation, increased glucose tolerance, and are almost entirely protected from hepatic steatosis, although, they gain fat mass similar to wild-type mice. Sirt1super mice are protected from liver cancer promoted by high-fat diet,
but are prone to thyroid and prostate cancer in combination with Pten-deficiency. Sirt1super mice have a normal longevity but some aging-associated phenotypes are improved.

Sirt1super mice have a threefold increase in SIRT1 expression directed by its endogenous promoter/enhancer regions on a BAC transgene. They may be useful when studying telomere deacetylation, DNA repair, energy homeostasis.

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