Cover

Mechanisms of Dietary Restriction in Aging and Disease

Editor(s): Mobbs C.V. (New York, N.Y.) 
Yen K. (New York, N.Y.) 
Hof P.R. (New York, N.Y.) 
Table of Contents
Vol. 35, No. , 2007
Section title: Paper
Free Access
Mobbs CV, Yen K, Hof PR (eds): Mechanisms of Dietary Restriction in Aging and Disease. Interdiscipl Top Gerontol. Basel, Karger, 2007, vol 35, pp 39-68
(DOI:10.1159/000096555)

Secrets of the lac Operon

Glucose Hysteresis as a Mechanism in Dietary Restriction, Aging and Disease

Mobbs C. · Mastaitis J. · Zhang M. · Isoda F. · Cheng H. · Yen K.
Departments of Neuroscience and Geriatrics, Mount Sinai School of Medicine, New York, N.Y., USA

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Abstract

Elevated blood glucose associated with diabetes produces progressive and apparently irreversible damage to many cell types. Conversely, reduction of glucose extends life span in yeast, and dietary restriction reduces blood glucose. Therefore it has been hypothesized that cumulative toxic effects of glucose drive at least some aspects of the aging process and, conversely, that protective effects of dietary restriction are mediated by a reduction in exposure to glucose. The mechanisms mediating cumulative toxic effects of glucose are suggested by two general principles of metabolic processes, illustrated by the lac operon but also observed with glucose-induced gene expression. First, metabolites induce the machinery of their own metabolism. Second, induction of gene expression by metabolites can entail a form of molecular memory called hysteresis. When applied to glucose-regulated gene expression, these two principles suggest a mechanism whereby repetitive exposure to postprandial excursions of glucose leads to an age-related increase in glycolytic capacity (and reduction in Β-oxidation of free fatty acids), which in turn leads to an increased generation of oxidative damage and a decreased capacity to respond to oxidative damage, independent of metabolic rate. According to this mechanism, dietary restriction increases life span and reduces pathology by reducing exposure to glucose and therefore delaying the development of glucose-induced glycolytic capacity.


Article / Publication Details

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Abstract of Paper

Published online: 10/20/2006
Cover Date: 2007

Number of Print Pages: 30
Number of Figures: 0
Number of Tables: 0

ISBN: 978-3-8055-8170-7 (Print)
eISBN: 978-3-318-01390-0 (Online)


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