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System-wide Benefits of Intermeal Fasting by Autophagy

Lookup NU author(s): Dr Nuria Martinez Lopez, Professor Rajat Singh

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Abstract

© 2017 Elsevier Inc. Autophagy failure is associated with metabolic insufficiency. Although caloric restriction (CR) extends healthspan, its adherence in humans is poor. We established an isocaloric twice-a-day (ITAD) feeding model wherein ITAD-fed mice consume the same food amount as ad libitum controls but at two short windows early and late in the diurnal cycle. We hypothesized that ITAD feeding will provide two intervals of intermeal fasting per circadian period and induce autophagy. We show that ITAD feeding modifies circadian autophagy and glucose/lipid metabolism that correlate with feeding-driven changes in circulating insulin. ITAD feeding decreases adiposity and, unlike CR, enhances muscle mass. ITAD feeding drives energy expenditure, lowers lipid levels, suppresses gluconeogenesis, and prevents age/obesity-associated metabolic defects. Using liver-, adipose-, myogenic-, and proopiomelanocortin neuron-specific autophagy-null mice, we mapped the contribution of tissue-specific autophagy to system-wide benefits of ITAD feeding. Our studies suggest that consuming two meals a day without CR could prevent the metabolic syndrome. Our studies suggest that consuming two meals a day with complete food restriction in between the meals is sufficient to lower blood glucose and lipid levels. This simple dietary approach activates a cell “cleansing system“ called autophagy in liver, fat, brain, and muscle that helps prevent obesity and diabetes.

Publication metadata

Author(s): Martinez-Lopez N, Tarabra E, Toledo M, Garcia-Macia M, Sahu S, Coletto L, Batista-Gonzalez A, Barzilai N, Pessin JE, Schwartz GJ, Kersten S, Singh R

Publication type: Article

Publication status: Published

Journal: Cell Metabolism

Year: 2017

Volume: 26

Issue: 6

Pages: 856-871.e5

Print publication date: 05/12/2017

Online publication date: 26/10/2017

Acceptance date: 25/09/2017

ISSN (print): 1550-4131

ISSN (electronic): 1932-7420

Publisher: Cell Press

URL: https://doi.org/10.1016/j.cmet.2017.09.020

DOI: 10.1016/j.cmet.2017.09.020

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