The prevalence of IGT and NIDDM in women with PCOS is substantially higher than expected when compared with age- and weight-matched populations of women without PCOS. The conversion from IGT to NIDDM is accelerated in PCOS. The fasting glucose concentration does not reliably predict the glucose concentration at 2 h after an oral glucose challenge, particularly among those with IGT, the subgroup at highest risk for subsequent development of NIDDM. We conclude that women with PCOS should periodically have an OGTT and must be closely monitored for deterioration in glucose tolerance.

Background Short sleep is associated with obesity and may alter the endocrine regulation of hunger and appetite. Objective To test the hypothesis that the curtailment of human sleep could promote excessive energy intake. Design Eleven healthy volunteers (5F/6M; mean ± SD age 39 ± 5y; BMI 26.5 ± 1.5 kg/m2) completed in random order two 14-day stays in the sleep laboratory with ad lib access to palatable food and 5.5- or 8.5-hour bedtimes. The primary endpoints were the calories from meals and snacks consumed during each bedtime condition. Additional measures included total energy expenditure and 24-hour profiles of serum leptin and ghrelin. Results Sleep was reduced by 122 ± 25 min/night during the 5.5-hour bedtime condition. While meal intake remained similar (P=0.51), sleep restriction was accompanied by increased consumption of calories from snacks (1087 ± 541 vs. 866 ± 365 kcal/day; P=0.026) with higher carbohydrate content (65 vs. 61%; P=0.04), particularly during the period from 19:00 to 7:00. These changes were not associated with a significant increase in energy expenditure during the 5.5-h (2526 ± 537 kcal/d) vs. 8.5-h bedtime period (2390 ± 369 kcal/d, P=0.58) and there were no significant differences in serum leptin and ghrelin between the two sleep conditions. Conclusions The results indicate that recurrent bedtime restriction can modify the amount, composition, and distribution of human food intake, and support the notion that sleeping short hours in an obesity-promoting environment may facilitate the excessive consumption of energy from snacks, but not meals.

Background Sleep loss can modify energy intake and expenditure. Objective To determine whether sleep restriction attenuates the effect of reduced-calorie diet on excess adiposity. Design Randomized two-period two-condition crossover study. Setting University clinical research center and sleep laboratory. Patients 10 overweight nonsmoking adults (3F/7M); mean (SD) age 41 (5) y; body mass index 27.4 (2.0) kg/m2. Intervention 14 days of moderate caloric restriction with 8.5 or 5.5-hour nighttime sleep opportunity. Measurements Primary: loss of fat and fat-free body mass. Secondary: changes in substrate utilization, energy expenditure, hunger, and 24-h metabolic hormone concentrations. Results Sleep curtailment decreased the fraction of weight lost as fat by 55% (1.4 vs. 0.6 kg with 8.5 vs. 5.5-h sleep opportunity, P=0.043) and increased the loss of fat-free body mass by 60% (1.5 vs. 2.4 kg, P=0.002). This was accompanied by markers of enhanced neuroendocrine adaptation to caloric restriction, increased hunger, and a shift in relative substrate utilization towards oxidation of less fat. Limitations The nature of the study limited its duration and sample size. Conclusions The amount of human sleep contributes to the maintenance of fat-free body mass at times of decreased energy intake. Lack of sufficient sleep may compromise the efficacy of typical dietary interventions for weight loss and related metabolic risk reduction.

Experimental bedtime restriction, designed to approximate the short sleep times experienced by many individuals in Westernized societies, may facilitate the development of insulin resistance and reduced glucose tolerance.

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