E. Vancauter et al., ABNORMAL TEMPORAL PATTERNS OF GLUCOSE-TOLERANCE IN OBESITY - RELATIONSHIP TO SLEEP-RELATED GROWTH-HORMONE SECRETION AND CIRCADIAN CORTISOL RHYTHMICITY, The Journal of clinical endocrinology and metabolism, 79(6), 1994, pp. 1797-1805
To define the chronobiology of glucose tolerance and insulin secretion
in obesity, nine obese men and nine lean men were studied during cons
tant glucose infusion for 53 h, including 8 h of nocturnal sleep, 28 h
of continuous wakefulness, and 8 h of daytime sleep. Blood samples we
re collected at 20-min intervals to assay glucose, insulin, C-peptide,
cortisol, and GH. Sleep was polygraphically monitored. Abnormal tempo
ral profiles of glucose regulation were observed during wakefulness an
d sleep in obese subjects. During daytime hours, the normal profile of
glucose tolerance was reversed, as an improvement, rather than a dete
rioration, was observed from morning to late evening. This reversal of
the daytime pattern appeared to be caused by a dual defect in glucose
regulation during the previous night. Indeed, during early sleep, GH
secretion was markedly reduced, and the nocturnal rises of glucose and
insulin secretion were dampened. During late sleep, obese subjects fa
iled to suppress insulin secretion and plasma glucose, resulting in hi
gh morning levels. Comparisons of metabolic and hormonal patterns duri
ng nocturnal and daytime sleep suggest that the failure to suppress in
sulin secretion in late sleep may reflect a relative insensitivity of
the beta-cell to acute inhibitory effects of cortisol in addition to i
nsulin resistance.