An open access paper: "The amount of fat mass of an organism is emerging as key determinant in longevity. Too little or too much fat is associated with early mortality in rodents and humans, whereas leanness, intermediate with respect to these two extremes is associated with relative longevity, possibly reflecting an optimal amount of fat. ... 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-aged Dgat1-/- 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."
30
Jan
2012
Another Mouse Longevity Mutation
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First Steps
The Causes of Aging
- Accumulating AGEs
- Buildup of Amyloid Between Cells
- The Failing Adaptive Immune System
- The Failing Innate Immune System
- Declining Lysosomal Function
- Mitochondrial DNA Damage
- Nuclear DNA Damage
- Buildup of Senescent Cells
- Other Causes of Aging
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Required Reading
- Calorie Restriction
- The Community, Visualized
- Cryonics
- Engineered Negligible Senescence
- Envisaging a World Without the FDA
- How to Argue for Longevity Science
- Introductory Articles
- The Odds of Human Longevity Mutations
- The Need For Activism and Advocacy
- Stem Cells, Regenerative Medicine
- Twelve Ways to Extend Mouse Life Span
- Transhumanism and Human Longevity
- The Vital Debate in Aging Research
- What is Anti-Aging?
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