Serum from Calorie-Restricted Rats Activates Vascular Cell eNOS through Enhanced Insulin Signaling Mediated by Adiponectin

被引：16
作者：
Cerqueira, Fernanda M. [1 ]
Brandizzi, Laura I. [2 ]
Cunha, Fernanda M. [1 ,3 ]
Laurindo, Francisco R. M. [2 ]
Kowaltowski, Alicia J. [1 ]
机构：
[1] Univ Sao Paulo, Inst Quim, Dept Bioquim, BR-01498 Sao Paulo, Brazil
[2] Univ Sao Paulo, Fac Med, Inst Coracao, Sao Paulo, Brazil
[3] Univ Sao Paulo, Escola Artes Ciencias & Humanidades, Sao Paulo, Brazil
来源：
PLOS ONE | 2012年 / 7卷 / 02期
基金：
巴西圣保罗研究基金会;
关键词：
NITRIC-OXIDE SYNTHASE; PROTEIN-KINASE-B; ENDOTHELIAL-CELLS; MITOCHONDRIAL BIOGENESIS; AKT; GLUCOSE; PHOSPHORYLATION; EXPRESSION; AGE; ADIPOCYTES;
D O I：
10.1371/journal.pone.0031155
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
eNOS activation resulting in mitochondrial biogenesis is believed to play a central role in life span extension promoted by calorie restriction (CR). We investigated the mechanism of this activation by treating vascular cells with serum from CR rats and found increased Akt and eNOS phosphorylation, in addition to enhanced nitrite release. Inhibiting Akt phosphorylation or immunoprecipitating adiponectin (found in high quantities in CR serum) completely prevented the increment in nitrite release and eNOS activation. Overall, we demonstrate that adiponectin in the serum from CR animals increases NO center dot signaling by activating the insulin pathway. These results suggest this hormone may be a determinant regulator of the beneficial effects of CR.
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页数：6
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