Independent Circadian and Sleep/Wake Regulation of Adipokines and Glucose in Humans
Steven A. Shea,
Michael F. Hilton,
Christine Orlova,
R. Timothy Ayers and
Christos S. Mantzoros
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 inregulating appetite, food intake, and energy balance and havepathophysiological roles in obesity and anorexia nervosa. Toassess the relative contributions of day/night patterns in behaviors(sleep/wake cycle and food intake) and of the endogenous circadianpacemaker on observed day/night patterns of adipokines, in sixhealthy subjects we measured circulating leptin, soluble leptinreceptor, adiponectin, glucose, and insulin levels throughouta constant routine protocol (38 h of wakefulness with constantposture, temperature, and dim light, as well as identical snacksevery 2 h) and throughout sleep and fasting periods before andafter the constant routine. There were significant endogenouscircadian rhythms in leptin, glucose, and insulin, with peaksaround the usual time of awakening. Sleep/fasting resulted inadditional systematic decreases in leptin, glucose, and insulin,whereas wakefulness/food intake resulted in a systematic increasein leptin. Thus, the day/night pattern in leptin is likely causedby combined effects from the endogenous circadian pacemakerand day/night patterns in behaviors. Our data imply that alterationsin the sleep/wake schedule would lead to an increased dailyrange in circulating leptin, with lowest leptin upon awakening,which, by influencing food intake and energy balance, couldbe implicated in the increased prevalence of obesity in theshift work population.
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