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Neurobiol Aging. 2015 Jul;36(7):2296-2303. doi: 10.1016/j.neurobiolaging.2015.03.012. Epub 2015 Mar 25.

Caloric restriction increases ketone bodies metabolism and preserves blood flow in aging brain.

Author information

1
Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA; Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY, USA. Electronic address: ailing.lin@uky.edu.
2
Research Imaging Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
3
Institutional Mass Spectrometry Laboratory, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA; Department of Biochemistry, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
4
Research Imaging Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA; Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.

Abstract

Caloric restriction (CR) has been shown to increase the life span and health span of a broad range of species. However, CR effects on in vivo brain functions are far from explored. In this study, we used multimetric neuroimaging methods to characterize the CR-induced changes of brain metabolic and vascular functions in aging rats. We found that old rats (24 months of age) with CR diet had reduced glucose uptake and lactate concentration, but increased ketone bodies level, compared with the age-matched and young (5 months of age) controls. The shifted metabolism was associated with preserved vascular function: old CR rats also had maintained cerebral blood flow relative to the age-matched controls. When investigating the metabolites in mitochondrial tricarboxylic acid cycle, we found that citrate and α-ketoglutarate were preserved in the old CR rats. We suggest that CR is neuroprotective; ketone bodies, cerebral blood flow, and α-ketoglutarate may play important roles in preserving brain physiology in aging.

KEYWORDS:

Aging; Brain metabolism; Cerebral blood flow; Ketone bodies; Mammalian target of rapamycin; Neuroimaging; α-ketoglutarate

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