Metabolic dysfunction is associated with circadian disturbances at both central and peripheral levels and, eventual disruption of circadian clock functioning can lead to obesity. Desynchronization between the central and peripheral clocks by altered timing of food intake and diet composition can lead to uncoupling of peripheral clocks from the central pacemaker and to the development of metabolic disorders.
The timing of three-meal schedules indicates close association with the plasma levels of insulin and preceding food availability. Fatty acids or their metabolites can modulate neuronal activity by brain nutrient-sensing neurons involved in the regulation of energy and glucose homeostasis. However, the hypothalamus has a crucial role in the regulation of energy balance rather than food intake. Food anticipatory activity is mediated by a self-sustained circadian timing and its principal component is food entrained oscillator. Its circadian rhythm is arranged with the predictable daily mealtimes. Food availability promotes the stimuli associated with food intake which is a circadian oscillator outside of the suprachiasmatic nucleus (SCN).
Dysfunction of these genes are involved in the alteration of these adipokines during the development of obesity. The clock genes and adipocytokines show circadian rhythmicity. The biological clocks of the circadian timing system coordinate cellular and physiological processes and synchronizes these with daily cycles, feeding patterns also regulates circadian clocks.
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