Leptin Levels Are Dependent on Sleep Duration: Relationships with Sympathovagal Balance, Carbohydrate Regulation, Cortisol, and Thyrotropin

Abstract

Sleep plays an important role in energy homeostasis. The present study tests the hypothesis that circulating levels of leptin, a hormone that signals energy balance to the brain, are influenced by sleep duration. We also analyzed associations between leptin and sympathovagal balance, cortisol, TSH, glucose, and insulin under different bedtime conditions. Twenty-four-hour hormonal and glucose profiles were sampled at frequent intervals, and sympathovagal balance was estimated from heart rate variability in 11 subjects studied after 6 d of 4-h bedtimes (mean +/- sem of sleep duration during last 2 d: 3 h and 49 +/- 2 min) and after 6 d of 12-h bedtimes (sleep: 9 h and 03 +/- 15 min). A study with 8-h bedtimes was performed 1 yr later (sleep: 6 h and 52 +/- 10 min). Caloric intake and activity levels were carefully controlled in all studies. Mean levels, maximal levels, and rhythm amplitude of leptin were decreased (-19%, -26%, and -20%, respectively) during sleep restriction compared with sleep extension. The decrease in leptin levels was concomitant with an elevation of sympathovagal balance. The effects of sleep duration on leptin were quantitatively associated with alterations of the cortisol and TSH profiles and were accompanied by an elevation of postbreakfast homeostasis model assessment values. Measures of perceived stress were not increased during sleep restriction. During the study with 8-h bedtimes, hormonal and metabolic parameters were intermediate between those observed with 4-h and 12-h bedtimes. In conclusion, sleep modulates a major component of the neuroendocrine control of appetite.

Factors associated with short and long sleep

“…These chronic health conditions could cause short sleep because of discomfort, pain and/or the side effects of medication (Moldofsky, 2001). Some longitudinal data also demonstrate that short sleep could contribute to these conditions (Ayas et al, 2003, Gangwisch et al, 2005, Gangwisch et al, 2006, Patel et al, 2006a, Patel et al, 2006b, Chaput et al, 2008and Shankar et al, 2008 possibly by altering sympathetic nervous system activity, neuroendocrine function and/or hypothalamic-pituitary-adrenal axis activity (Leproult et al, 1997, Spiegel et al, 2004and Van Cauter et al, 2007. However, more research is required to investigate the role of short sleep as a risk factor for chronic disease.…”

Sleep-related disturbances and physical inactivity are independently associated with obesity in adults

“…A causative path from sleep and circadian clock system to obesity has been suggested through direct metabolic (see for example Kohsaka et al 17 and Kohsaka and Bass 18 ) and/or hormonal changes with an influence on energy intake. 14,19 More indirect pathways are also plausible, for instance, short or disturbed sleep may cause fatigue leading to restriction of physical activity. Physical inactivity may, in turn, have a negative feed-back effect on sleep.…”

Upregulation of Gene Expression in Reward-Modulatory Striatal Opioid Systems by Sleep Loss

“…There is much interest in identifying the physiological basis of these behavioral changes, and studies to date have focused mainly on peripheral endocrine systems (eg, leptin and ghrelin) that regulate feeding in conjunction with energy-balance fluctuations. In some human studies, leptin and ghrelin levels are altered in sleep loss in directions that promote food intake, and rodent studies have shown that sleep curtailment modulates hypothalamic peptides and other systems whose activity tracks these circulating hormones (Barf et al, 2012;Koban et al, 2006;Martins et al, 2010;Spiegel et al, 2004b).…”