Author:
Kooijman Sander,van den Berg Rosa,Ramkisoensing Ashna,Boon Mariëtte R.,Kuipers Eline N.,Loef Marieke,Zonneveld Tom C. M.,Lucassen Eliane A.,Sips Hetty C. M.,Chatzispyrou Iliana A.,Houtkooper Riekelt H.,Meijer Johanna H.,Coomans Claudia P.,Biermasz Nienke R.,Rensen Patrick C. N.
Abstract
Disruption of circadian rhythmicity is associated with obesity and related disorders, including type 2 diabetes and cardiovascular disease. Specifically, prolonged artificial light exposure associates with obesity in humans, although the underlying mechanism is unclear. Here, we report that increasing the daily hours of light exposure increases body adiposity through attenuation of brown adipose tissue (BAT) activity, a major contributor of energy expenditure. Mice exposed to a prolonged day length of 16- and 24-h light, compared with regular 12-h light, showed increased adiposity without affecting food intake or locomotor activity. Mechanistically, we demonstrated that prolonged day length decreases sympathetic input into BAT and reduces β3-adrenergic intracellular signaling. Concomitantly, prolonging day length decreased the uptake of fatty acids from triglyceride-rich lipoproteins, as well as of glucose from plasma selectively by BAT. We conclude that impaired BAT activity is an important mediator in the association between disturbed circadian rhythm and adiposity, and anticipate that activation of BAT may overcome the adverse metabolic consequences of disturbed circadian rhythmicity.
Funder
Nederlandse Organisatie voor Wetenschappelijk Onderzoek
European Foundation for the Study of Diabetes
Diabetes Fonds
Hartstichting
Publisher
Proceedings of the National Academy of Sciences
Cited by
115 articles.
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