ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2008) 16 P391

Nocturnal HPA axis activity is blunted by increased plasma glucose concentrations

Christian Benedict1, Manfred Hallschmid1, Werner Kern3, Bernd Schultes2, Hendrik Lehnert3 & Jan Born1


1Department of Neuroendocrinology, University of Lübeck, Lübeck, Germany; 2Interdisciplinary Obesity Center East-Switzerland, Kantonsspital St Gallen, St Gallen, Switzerland; 3Internal Medicine I, University of Lübeck, Lübeck, Germany.


Background: Secretory activity of the hypothalamo-pituitary–adrenal (HPA) axis typically increases during the second half of nocturnal sleep. Assuming that this rise in ACTH and cortisol levels occurs in response to the negative energy balance induced by nocturnal fasting and concomitant increases in cerebral glucose consumption during REM sleep, we examined the effects of glucose infusion on nocturnal HPA axis activity during wake and sleep periods.

Methods and findings: According to a 2×2 design, healthy men were infused with glucose (4.5 mg/kg×min) and saline, respectively, during sleep (n=9) or total sleep deprivation (n=11). Circulating concentrations of ACTH, cortisol, glucose, insulin, and leptin were measured and food consumption from a breakfast buffet presented on the subsequent morning was assessed. Independent of sleep, nocturnal secretion of ACTH and cortisol was suppressed by glucose infusion (glucose vs saline: ACTH, 11.93±0.77 vs 13.60±1.08 pg/ml; cortisol, 5.21±0.92 vs 7.20±0.79 μg/dl; each P<0.05). In the sleep group, glucose infusion enhanced REM sleep while reducing the time spent in sleep stage 2 (each P<0.05). Sleep deprivation per se was associated with a reduction in leptin levels compared to sleep (P<0.05). Following nocturnal glucose infusion, food intake was reduced in comparison to placebo in the wake but not in the sleep group (P<0.05 and P>0.82, respectively).

Conclusions: Our findings indicate that nocturnal HPA axis activity is blunted by increased plasma glucose concentrations, suggesting that the brain regulates nocturnal ACTH and cortisol release in response to the level of energy available in the form of blood glucose. Sleep does not appear to be critically involved in this glucose/glucocorticoid feedback loop.

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