Sleep deprivation may prevent counterregulatory adaptation to recurrent hypoglycemia
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In a cohort of healthy young adult men, one night of sleep deprivation attenuated the adaptation to recurrent hypoglycemia by preserving neuroendocrine counterregulation and subjective awareness, according to study findings.
“Hypoglycemia unawareness is often observed in clinical practice, and elderly patients are at a particular risk because subjective awareness of hypoglycemia decreases with age despite unchanged neuroendocrine counterregulation,” Svenja Meyhöfer, MD, of the Institute for Endocrinology and Diabetes at the University of Lübeck in Germany, and colleagues wrote in a study published in Diabetologia. “Improving subjective awareness of hypoglycemia is key for patients with diabetes to break the vicious cycle of undetected severe hypoglycemic episodes and the resulting adaptation-induced hypoglycemia unawareness. Our results indicate that sleep deprivation is able to preserve neuroendocrine counterregulation and subjective awareness in response to recurrent hypoglycemia in an acute setting. They call for investigations into the role of sleep-related processes in chronic hypoglycemia unawareness that may open new perspectives for prevention of this debilitating complication of diabetes treatment.”
Researchers conducted a balanced, crossover study with 15 healthy men aged 18 to 35 years with normal weight. The cohort participated in two randomly scheduled experimental sessions. Both sessions began in the morning of day 1 and concluded in the morning of day 2. One session had participants sleep from 11 p.m. on day 1 until 7 a.m. on day 2, and the second session required participants to be sleep deprived and stay awake all night with a fixed repertoire of movies and games. Hypoglycemic clamps were performed in the morning and afternoon of day 1. A third hypoglycemic clamp was performed in the morning of day 2 after sleep or sleep deprivation. Subjective symptoms of hypoglycemia were assessed through a questionnaire.
Participants had a dampened neuroendocrine adaptation to recurrent hypoglycemia in the sleep deprivation state compared with regular sleep. The increase in concentration of adrenaline during hypoglycemia was attenuated during the third clamp for men in the sleep condition but was maintained during sleep deprivation (P = .004). The same pattern was observed with growth hormone (P = .029), but there was no significant difference with glucagon. Adrenaline, growth hormone and glucagon largely corroborated the attenuating effect of sleep deprivation on adaptation to recurrent hypoglycemia (P = .064).
There was a significant decrease in adrenocorticotropic hormone (ACTH) levels during the maximal counterregulatory response between the first hypoglycemia clamp and the final clamp during the sleep condition (P = .04), but no difference was found during sleep deprivation. No differences between the first and final clamps were observed for noradrenaline concentrations during either sleep condition.
Men reported attenuated neuroglycopenic symptoms after regular sleep compared with sleep deprivation (P < .05). There was a significant reduction in neuroglycopenic symptoms in the final hypoglycemic clamp compared with the first during the sleep condition (P = .005), whereas symptoms increased in the final clamp compared with the first after sleep deprivation (P = .014). Autonomic symptoms decreased in the final clamp during the sleep condition compared with the first clamp (P = .019), but no difference was observed after sleep deprivation.
The researchers said more studies should be conducted in other populations to confirm the findings.
“Our experiments were performed in a small group of healthy men. Although we do not expect gender differences, we cannot rule out the possibility that the observed effects may be more or less pronounced in women,” the researchers wrote. “Moreover, the study should be repeated in patients with diabetes. Future studies are also needed to identify the mechanisms underlying the effect of sleep deprivation on the adaptation to recurrent hypoglycemia and to single out the contribution of direct effects on counterregulatory processes.”
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