Interactions between metabolism and circadian clocks: reciprocal disturbances.
Obesity is a medical condition of excess body fat, recognized as a global epidemic. Besides genetic factors, overconsumption of high-energy food and a sedentary lifestyle are major obesogenic causes. A newly identified determinant is altered circadian rhythmicity. To anticipate and adapt to daily changes in the environment, organisms have developed an endogenous circadian timing system, comprising a main circadian clock, located in the suprachiasmatic nucleus (SCN) of the hypothalamus, principally synchronized to the light-dark cycle. Secondary peripheral clocks are found in various tissues, such as the liver, pancreas, and adipose tissue. These clocks control the rhythmic patterns of myriad metabolic processes. We will review the evidence that metabolic dysfunction is associated with circadian disturbances at both central and peripheral levels and, conversely, that disruption of circadian clock functioning can lead to obesity. The roots of these reciprocal interactions will be illustrated by transcriptional crosstalk between metabolic and circadian systems. Chronotherapeutic approaches of dieting to maintain or restore a proper circadian alignment could be useful to limit the magnitude of metabolic risks.
Department of Neurobiology of Rhythms, Institute of Cellular and Integrative Neurosciences, Centre National de la Recherche Scientifique, UPR3212, University of Strasbourg, Strasbourg, France.
Julien
J
Delezie
Etienne
E
Challet
D000818:Animals; D021081:Chronobiology Disorders / Q000150:complications / Q000235:genetics / Q000378:metabolism; D057906:Circadian Clocks / Q000235:genetics / Q000502:physiology*; D048909:Diabetes Complications / Q000378:metabolism; D006801:Humans; D053858:Metabolic Networks and Pathways; D008954:Models, Biological; D009765:Obesity / Q000150:complications / Q000235:genetics / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism
D018160:Receptors, Cytoplasmic and Nuclear