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

Aging (Albany NY). 2012 Jan;4(1):13-27. doi: 10.18632/aging.100424.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / physiology
  • Aging / metabolism
  • Animals
  • Body Composition
  • Bone Density / genetics
  • Bone Density / physiology
  • Caloric Restriction
  • Diacylglycerol O-Acyltransferase / deficiency
  • Diacylglycerol O-Acyltransferase / genetics
  • Diacylglycerol O-Acyltransferase / metabolism*
  • Energy Metabolism / genetics
  • Energy Metabolism / physiology
  • Female
  • Fertility
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Genotype
  • Litter Size
  • Longevity / genetics*
  • Longevity / physiology*
  • Mice
  • Mice, Knockout
  • Thinness / enzymology
  • Thinness / metabolism

Substances

  • Dgat1 protein, mouse
  • Diacylglycerol O-Acyltransferase