Journal
INTERNATIONAL JOURNAL OF OBESITY
Volume 30, Issue 1, Pages 60-67Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.ijo.0803048
Keywords
dietary obesity; leptin; insulin; circadian rhythms; synchronization
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Objective: To assess whether circadian desynchronization leads to metabolic alterations capable of promoting dietary obesity and/or impairing glucose tolerance. Design: Rats fed either with chow pellets (i.e., low-fat diet with 4% mass of fat) or high-fat diet (34% mass of fat). Half of each diet group was exposed to a fixed light-dark cycle or to a 10-h weekly shift in the light-dark cycle from Thursday to Sunday (20 shifts). To enforce the shifted animals to be active at unusual times of the day, food was available only during the daily dark period for all groups. Results: Shifting the light-dark cycle on a weekly basis was efficient to induce circadian desynchronization, as evidenced by strong disturbances in the daily expression of locomotor activity. Shifted rats fed with a nocturnal low-fat diet had lower plasma insulin and similar blood glucose compared to rats fed with the same diet under a fixed light-dark cycle. Nocturnal high-fat feeding led to an abdominal fat overload associated with increased plasma leptin and basal glucose. These metabolic changes were not significantly modified by circadian desynchronization. Conclusion: Chronic desynchronization with low-fat diet impaired insulin regulation. Metabolic changes induced by the high-fat diet were not aggravated by chronic desynchronization.
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