eNOS activation resulting in mitochondrial biogenesis is believed to play a central role in life span extension promoted by\ncalorie restriction (CR). We investigated the mechanism of this activation by treating vascular cells with serum from CR rats\nand found increased Akt and eNOS phosphorylation, in addition to enhanced nitrite release. Inhibiting Akt phosphorylation\nor immunoprecipitating adiponectin (found in high quantities in CR serum) completely prevented the increment in nitrite\nrelease and eNOS activation. Overall, we demonstrate that adiponectin in the serum from CR animals increases NON\nsignaling by activating the insulin pathway. These results suggest this hormone may be a determinant regulator of the\nbeneficial effects of CR.
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