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Independent Circadian and Sleep/Wake Regulation of Adipokines and Glucose in Humans

Medical Chronobiology Program (S.A.S., M.F.H., R.T.A.), Brigham and Women’s Hospital, Boston, Massachusetts 02115; Harvard Medical School (S.A.S., M.F.H., C.S.M.), Boston, Massachusetts 02115; Division of Endocrinology, Diabetes, and Metabolism (C.O., C.S.M.), Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215

Address all correspondence and requests for reprints to: Steven A. Shea, Ph.D., Medical Chronobiology Program, Brigham and Women’s Hospital, Sleep Disorders Research Program at Beth Israel Deaconess Medical Center, 75 Francis Street, Boston, Massachusetts 02115. E-mail: sshea{at}hms.harvard.edu; or Christos S. Mantzoros, M.D., Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Stoneman 816, Boston, Massachusetts 02215. E-mail: cmantzor{at}bidmc.harvard.edu.

Leptin and adiponectin play important physiological roles in regulating appetite, food intake, and energy balance and have pathophysiological roles in obesity and anorexia nervosa. To assess the relative contributions of day/night patterns in behaviors (sleep/wake cycle and food intake) and of the endogenous circadian pacemaker on observed day/night patterns of adipokines, in six healthy subjects we measured circulating leptin, soluble leptin receptor, adiponectin, glucose, and insulin levels throughout a constant routine protocol (38 h of wakefulness with constant posture, temperature, and dim light, as well as identical snacks every 2 h) and throughout sleep and fasting periods before and after the constant routine. There were significant endogenous circadian rhythms in leptin, glucose, and insulin, with peaks around the usual time of awakening. Sleep/fasting resulted in additional systematic decreases in leptin, glucose, and insulin, whereas wakefulness/food intake resulted in a systematic increase in leptin. Thus, the day/night pattern in leptin is likely caused by combined effects from the endogenous circadian pacemaker and day/night patterns in behaviors. Our data imply that alterations in the sleep/wake schedule would lead to an increased daily range in circulating leptin, with lowest leptin upon awakening, which, by influencing food intake and energy balance, could be implicated in the increased prevalence of obesity in the shift work population.

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