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Deficiency of the lipid synthesis enzyme, DGAT1, extends longevity in mice.

Ryan S Streeper | Carrie A Grueter | Nathan Salomonis | Sylvaine Cases | Malin C Levin | Suneil K Koliwad | Ping Zhou | Mattew D Hirschey | Eric Verdin | Robert V Farese
Aging | 2012

Calorie restriction results in leanness, which is linked to metabolic conditions that favor longevity. We show here that deficiency of the triglyceride synthesis enzyme acyl CoA:diacylglycerol acyltransferase 1 (DGAT1), which promotes leanness, also extends longevity without limiting food intake. Female DGAT1-deficient mice were protected from age-related increases in body fat, tissue triglycerides, and inflammation in white adipose tissue. This protection was accompanied by increased mean and maximal life spans of ~25% and ~10%, respectively. Middle-agedDgat1-/- mice exhibited several features associated with longevity, including decreased levels of circulating insulin growth factor 1 (IGF1) and reduced fecundity. Thus, deletion of DGAT1 in mice provides a model of leanness and extended lifespan that is independent of calorie restriction.

Pubmed ID: 22291164

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Associated grants

  • Agency: NCRR NIH HHS, United States
    Id: C06 RR018928
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK056084
  • Agency: NCI NIH HHS, United States
    Id: CO6 RR18928
  • Agency: NIDDK NIH HHS, United States
    Id: R01-DK056084

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LIMMA (tool)

RRID:SCR_010943

Software package for the analysis of gene expression microarray data, especially the use of linear models for analyzing designed experiments and the assessment of differential expression.

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C57BL/6J (tool)

RRID:IMSR_JAX:000664

Mus musculus with name C57BL/6J from IMSR.

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