Caloric restriction impedes age-related decline of mitochondrial function and neuronal activity

被引：44

作者：

Lin, Ai-Ling ^{[1
,2
]}

Coman, Daniel ^{[3
,4
,5
]}

Jiang, Lihong ^{[3
,4
,5
]}

Rothman, Douglas L. ^{[3
,4
,5
,6
]}

Hyder, Fahmeed ^{[3
,4
,5
,6
]}

机构：

[1] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40536 USA

[2] Univ Kentucky, Dept Pharmacol & Nutr Sci, Lexington, KY 40536 USA

[3] Yale Univ, Magnet Resonance Res Ctr, New Haven, CT USA

[4] Yale Univ, Quantitat Neurosci Magnet Resonance Core Ctr, New Haven, CT USA

[5] Yale Univ, Dept Diagnost Radiol, New Haven, CT 06510 USA

[6] Yale Univ, Dept Biomed Engn, New Haven, CT USA

来源：

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM | 2014年 / 34卷 / 09期

关键词：

aging; energy metabolism; mitochondria; neurophysiology; MR spectroscopy; RAT-BRAIN; LIFE-SPAN; IN-VIVO; GLUCOSE; NMR; BIOGENESIS; METABOLISM; ACTIVATION; DISEASE; ENERGY;

D O I：

10.1038/jcbfm.2014.114

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Caloric restriction (CR) prolongs lifespan and retards many detrimental effects of aging, but its effect on brain mitochondrial function and neuronal activity-especially in healthy aging-remains unexplored. Here we measured rates of neuronal glucose oxidation and glutamate-glutamine neurotransmitter cycling in young control, old control (i.e., healthy aging), and old CR rats using in vivo nuclear magnetic resonance spectroscopy. We found that, compared with the young control, neuronal energy production and neurotransmission rates were significantly reduced in healthy aging, but were preserved in old CR rats. The results suggest that CR mitigated the age-related deceleration of brain physiology.

引用

页码：1440 / 1443

页数：4

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