Calorie restriction induces mitochondrial biogenesis and bioenergetic efficiency

We have focused our research on a related, but different, antiaging mechanism of calorie restriction

G. L pez-Lluch; N. Hunt; B. Jones; M. Zhu; H. Jamieson; S. Hilmer; M. V. Cascajo; J. Allard; D. K. Ingram; P. Navas; R. de Cabo


Scholarcy highlights

  • One of the major hypotheses directing gerontological research over several decades is that aging results from the accumulation of macromolecules damaged by oxidative stress and that the major loci of this damage is the mitochondrion
  • Past studies have demonstrated that calorie restriction decreases mitochondrial electron and proton leak in mammalian cells and attenuates damage resulting from intracellular oxidative stress
  • Lifespan is inversely related to the rate of mitochondrial hydroperoxide production that has been reported to increase with aging and decrease with CR
  • To investigate whether the CR-dependent decrease of mitochondrial reactive oxygen species production is reproduced in vitro, HeLa cells, FaO cells, and primary hepatocytes were incubated in the presence of serum from rats submitted to long-term CR and compared with those incubated with serum from age-matched, ad libitum-fed rats
  • A significant decrease in ROS production in CR cells was observed when compared with cells grown in AL serum
  • Our results contradict the recent results of Lambert and Merry showing that CR did not affect bioenergetics or ROS production in intact rat hepatocytes isolated from CR rats. This discrepancy may be caused by differences in the dietary regimen and methods used for ROS determination in both studies and because we have treated cells in vitro with CR serum, whereas the hepatocytes in the Lambert and Merry study were isolated from CR rats and grown in Hanks’ balanced salt solution
  • Biochemical determination of mitochondrial mass was performed by measuring the citrate synthase activity in whole extracts from cells

Need more features? Save interactive summary cards to your Scholarcy Library.