Over the past decade, two startling health statistics have captured widespread public attention: first, that all children born in the year 2000 face a one-in-three chance of developing diabetes during their lifetime; second, that nearly one-third of the US population is overweight or obese.

Although sedentary habits and high fat diet are the most recognized factors in this epidemic, new evidence from both clinical studies in humans and experimental models has pinpointed a role for disruption in the circadian system and sleep in obesity and diabetes. Our focus is to dissect the molecular basis underlying metabolic and energy disorders in models of circadian disruption using a range of approaches from genetics, biochemistry, cell biology and physiology.

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