Reduced lifespan of mice lacking catalase correlates with altered lipid metabolism without oxidative damage or premature aging

Free Radical Biology & Medicine
José Raúl Pérez-EstradaLuis Covarrubias

Abstract

The relationship between the mechanisms that underlie longevity and aging and the metabolic alterations due to feeding conditions has not been completely defined. In the present work, through the deletion of the gene encoding catalase, hydrogen peroxide (H2O2) was uncovered as a relevant regulator of longevity and of liver metabolism. Mice lacking catalase (Cat-/-) fed ad libitum with a regular diet showed a shorter lifespan than wild type mice, which correlated with reduced body weight, blood glucose levels and liver fat accumulation, but not with increased oxidative damage or consistent premature aging. High fat diet (HFD) and fasting increased oxidative damage in the liver of wild type animals but, unexpectedly, this was not the case for that of Cat-/- mice. Interestingly, although HFD feeding similarly increased the body weight of Cat-/- and wild-type mice, hyperglycemia and liver steatosis did not develop in the former. Fat accumulation due to fasting, on the other hand, was diminished in mice lacking catalase, which correlated with increased risk of death and low ketone body blood levels. Alteration in expression of some metabolic genes in livers of catalase deficient mice was consistent with reduced lipogenesis. Specific...Continue Reading

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