Sleep loss alters basal metabolic hormone secretion and modulates the dynamic counterregulatory response to hypoglycemia.
BACKGROUND
Sleep loss has immediate effects on metabolic function that in the long run may contribute to the development of obesity and type 2 diabetes.


OBJECTIVE
Our objective was to explore the neuroendocrine mechanisms mediating the acute effects of sleep deprivation on blood glucose regulation under basal and hypoglycemic conditions.


METHODS
In a randomized, crossover study in 10 healthy young men, plasma concentrations of relevant hormones were examined during basal rest, a subsequent stepwise hypoglycemic clamp after one night of total sleep deprivation (SD) and one night of regular sleep.


RESULTS
Basal glucagon concentrations were decreased (P = 0.022) and C-peptide levels were slightly reduced after SD (P = 0.085), compared with regular sleep. During hypoglycemia after SD, the glucagon increase relative to baseline was enhanced (P = 0.034) and the relative decrease in C-peptide was reduced (P = 0.013). Also, the relative increase in norepinephrine was reduced (P = 0.031). SD did not affect epinephrine, ACTH, cortisol, lactate, beta-hydroxybutyrate, or nonesterified fatty acids during hypoglycemia, but overall, plasma nonesterified fatty acid levels were reduced after SD (P = 0.009). SD markedly increased rated hunger during basal rest (P < 0.008), resulting in a dampened relative increase during hypoglycemia (P < 0.009). Unexpectedly, despite distinct alterations in basal secretory activity, the absolute amplitude of hormonal counterregulation and hunger responses to hypoglycemia was not affected by SD.


CONCLUSIONS
Short-term SD distinctly alters hormonal glucose regulation, affecting especially pancreatic islet secretion, and also increases hunger. Immediate perturbations in the dynamic regulation of energy metabolism caused by acute sleep curtailment may contribute to the association between chronic sleep loss and metabolic disorders.
Schmid
Sebastian M
SM
Department of Internal Medicine, University of Luebeck, Germany.
Hallschmid
Manfred
M
Jauch-Chara
Kamila
K
Bandorf
Nadine
N
Born
Jan
J
Schultes
Bernd
B
D020155:3-Hydroxybutyric Acid / Q000097:blood; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D002096:C-Peptide / Q000097:blood; D018592:Cross-Over Studies; D004837:Epinephrine / Q000097:blood; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005934:Glucagon / Q000097:blood; D005947:Glucose / Q000494:pharmacology; D015309:Glucose Clamp Technique; D006728:Hormones / Q000097:blood / Q000378:metabolism*; D019382:Human Growth Hormone / Q000097:blood; D006801:Humans; D006815:Hunger / Q000502:physiology; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000378:metabolism* / Q000503:physiopathology; D019344:Lactic Acid / Q000097:blood; D008297:Male; D009490:Neurosecretory Systems / Q000378:metabolism* / Q000503:physiopathology; D009638:Norepinephrine / Q000097:blood; D012892:Sleep Deprivation / Q000378:metabolism* / Q000523:psychology
D002096:C-Peptide; D005230:Fatty Acids, Nonesterified; D006728:Hormones; D019382:Human Growth Hormone; D019344:Lactic Acid; D000324:Adrenocorticotropic Hormone; D005934:Glucagon; D005947:Glucose; D020155:3-Hydroxybutyric Acid; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine