In contrast to our expectation, short-term sleep loss neither increased food intake nor affected concentrations of the hunger-regulating hormones leptin and ghrelin. However, the observed decrease in daytime physical activity may point to another potentially important behavioral mechanism for the health-impairing influence of sleep loss.

Background: Voluntary sleep restriction is a lifestyle feature of modern societies that may contribute to obesity and diabetes. The aim of the study was to investigate the impact of partial sleep deprivation on the regulation of energy balance and insulin sensitivity. Subjects and Methods: In a controlled intervention, 14 healthy women (age 23–38 years, BMI 20.0–36.6 kg/m²) were investigated after 2 nights of >8 h sleep/night (T0), after 4 nights of consecutively increasing sleep curtailment (7 h sleep/ night, 6 h sleep/night, 6 h sleep/night and 4 h sleep/night; T1) and after 2 nights of sleep recovery (>8 h sleep/night; T2). Resting and total energy expenditure (REE, TEE), glucose-induced thermogenesis (GIT), physical activity, energy intake, glucose tolerance and endocrine parameters were assessed. Results: After a decrease in sleep du-ration, energy intake (+20%), body weight (+0.4 kg), leptin / fat mass (+29%), free triiodothyronine (+19%), free thyroxine (+10%) and GIT (+34%) significantly increased (all p < 0.05). Mean REE, physical activity, TEE, oral glucose tolerance, and ghrelin levels remained unchanged at T1. The effect of sleep loss on GIT, fT3 and fT4 levels was inversely related to fat mass. Conclusion: Short-term sleep deprivation increased energy intake and led to a net weight gain in women. The effect of sleep restriction on energy expenditure needs to be specifically addressed in future studies using reference methods for total energy expenditure.

SUMMAR Y Sleep loss is currently proposed to disturb endocrine regulation of energy homeostasis leading to weight gain and obesity. Supporting this view, a reduction of sleep duration to 4 h for two consecutive nights has recently been shown to decrease circulating leptin levels and to increase ghrelin levels, as well as self-reported hunger. We hypothesized that similar endocrine alterations occur even after a single night of sleep restriction. In a balanced order, nine healthy normal-weight men spent three nights in our sleep laboratory separated by at least 2 weeks: one night with a total sleep time of 7 h, one night with a total sleep time of 4.5 h and one night with total sleep deprivation (SD). On a standard symptom-rating scale, subjects rated markedly stronger feelings of hunger after total SD than after 7 h sleep (3.9 ± 0.7 versus 1.7 ± 0.3; P = 0.020) or 4.5 h sleep (2.2 ± 0.5; P = 0.041). Plasma ghrelin levels were 22 ± 10% higher after total SD than after 7 h sleep (0.85 ± 0.06 versus 0.72 ± 0.04 ng mL )1 ; P = 0.048) with intermediate levels of the hormone after 4.5 h sleep (0.77 ± 0.04 ng mL )1 ). Serum leptin levels did not differ between conditions. Feelings of hunger as well as plasma ghrelin levels are already elevated after one night of SD, whereas morning serum leptin concentrations remain unaffected. Thus, our results provide further evidence for a disturbing influence of sleep loss on endocrine regulation of energy homeostasis, which on the long run may result in weight gain and obesity.k e y w o r d s energy homeostasis, ghrelin, leptin, obesity, sleep loss

OBJECTIVEOlder patients with type 2 diabetes are at a particularly high risk for severe hypoglycemic episodes, and experimental studies in healthy subjects hint at a reduced awareness of hypoglycemia in aged humans. However, subjective responses to hypoglycemia have rarely been assessed in older type 2 diabetic patients.RESEARCH DESIGN AND METHODSWe tested hormonal, subjective, and cognitive responses (reaction time) to 30-min steady-state hypoglycemia at a level of 2.8 mmol/l in 13 older (≥65 years) and 13 middle-aged (39–64 years) type 2 diabetic patients.RESULTSHormonal counterregulatory responses to hypoglycemia did not differ between older and middle-aged patients. In contrast, middle-aged patients showed a pronounced increase in autonomic and neuroglycopenic symptom scores at the end of the hypoglycemic plateau that was not observed in older patients (both P < 0.01). Also, seven middle-aged patients, but only one older participant, correctly estimated their blood glucose concentration to be <3.3 mmol/l during hypoglycemia (P = 0.011). A profound prolongation of reaction times induced by hypoglycemia in both groups persisted even after 30 min of subsequent euglycemia.CONCLUSIONSOur data indicate marked subjective unawareness of hypoglycemia in older type 2 diabetic patients that does not depend on altered neuroendocrine counterregulation and may contribute to the increased probability of severe hypoglycemia frequently reported in these patients. The joint occurrence of hypoglycemia unawareness and deteriorated cognitive function is a critical factor to be carefully considered in the treatment of older patients.

Data indicate an impairment of glucose tolerance after 2 days of sleep restriction to ~4 h that appears to be primarily caused by a reduction in insulin sensitivity. Unchanged HPA secretory activity and IL-6 concentrations argue against a mediation of these effects by stress-related or inflammatory mechanisms.