On a HC diet, the subjects who had a higher positive CHO balance on day 15 while they were inactive gained less fat mass during 4 y, a predictive effect independent of S(I). As suggested in rodents, the capacity to expand the glycogen pool might reduce energy intake and protect against fat and weight gain.

Chronic consumption of a high-carbohydrate diet could provide some protection against body fat accumulation in persons with a pattern of physical activity that includes frequent sedentary days.

Adipose tissue lipoprotein lipase (ATLPL) provides free fatty acids (FFA) for storage in adipocytes, whereas in skeletal muscle LPL (SMLPL) provides FFA for oxidation. In hibernating animals, the level of SMLPL is relatively higher in summer than winter (promoting fat oxidation), whereas the opposite is seen with ATLPL. A patientcontrolled study was designed to determine whether such seasonal variation occurs in normal weight humans.Eighteen subjects were studied in the summer and winter. After 2 days of a standardized diet, they underwent muscle and adipose biopsies for LPL activity, assessment of fitness by V O 2 max, and determination of body composition by hydrostatic weighing. The percentages of body fat, body mass index, V O 2 max, insulin, glucose, FFA, glycerol, and leptin were not affected by the season. Total cholesterol was higher in the winter than in the summer (157 Ϯ 5.5 vs. 148 Ϯ 4.2 mg/dL respectively; P ϭ 0.03). The ATLPL activity was also higher in the winter than in the summer (4.4 Ϯ 0.8 vs. 2.3 Ϯ 0.6 nmol FFA/10 6 cells⅐min; P ϭ 0.04). SMLPL activity trended to be higher in the winter than in the summer (1.9 Ϯ 0.5 vs. 1.0 Ϯ 0.1 nmol FFA/g⅐min; P ϭ 0.06).In summary, ATLPL is seasonally regulated. It appears that SMLPL is similarly regulated by season. For physically active lean subjects, this increase in SMLPL may be a compensatory mechanism to help protect from seasonal weight gain. (J Clin Endocrinol Metab 85: [3065][3066][3067][3068] 2000)

The goals of the study were to determine if moderate weight loss in severely obese adults resulted in (i) reduction in apnea/hypopnea index (AHI), (ii) improved pharyngeal patency, (iii) reduced total body oxygen consumption (VO2) and carbon dioxide production (VCO2) during sleep, and (iv) improved sleep quality. The main outcome was the change in AHI from before to after weight loss. Fourteen severely obese (BMI > 40 kg/m2) patients (3 males, 11 females) completed a highly controlled weight reduction program which included 3 months of weight loss and 3 months of weight maintenance. At baseline and postweight loss, patients underwent pulmonary function testing, polysomnography, and magnetic resonance imaging (MRI) to assess neck morphology. Weight decreased from 134 ±6.6 kg to 118 ± 6.1 kg (mean ± s.e.m.; F = 113.763, P < 0.0001). There was a significant reduction in the AHI between baseline and postweight loss (subject, F = 11.11, P = 0.007). Moreover, patients with worse sleep‐disordered breathing (SDB) at baseline had the greatest improvements in AHI (group, F = 9.00, P = 0.005). Reductions in VO2 (285 ± 12 to 234 ±16 ml/min; F = 24.85, P < 0.0001) and VCO2 (231 ± 9 to 186 ± 12 ml/min; F = 27.74, P < 0.0001) were also observed, and pulmonary function testing showed improvements in spirometry parameters. Sleep studies revealed improved minimum oxygen saturation (minSaO2) (83.4 ± 61.9% to 89.1 ± 1.2%; F = 7.59, P = 0.016), and mean SaO2 (90.4 ± 1.1% to 93.8 ± 1.0%; F = 6.89, P = 0.022), and a significant increase in the number of arousals (8.1 ± 1.4 at baseline, to 17.1 ± 3.0 after weight loss; F = 18.13, P = 0.001). In severely obese patients, even moderate weight loss (∼10%) boasts substantial benefit in terms of the severity of SDB and sleep dynamics.

OBJECTIVES: After 10 d of orlistat administration (120 mg three timesaday), the primary objective was to determine the drug's effect on postprandial plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) activities on day 10 after an oral fat-load. The secondary objectives were to determine the effects of orlistat on 12 h postprandial measures of: (1) preheparin HTGL and LPL; and (2) serum triglycerides, very-low-density lipoprotein cholesterol, highdensity lipoprotein cholesterol, low-density lipoprotein cholesterol and free fatty acids. METHODS: Twenty-four normal-weight, healthy male volunteers were randomized to either 120 mg orlistat (n 12) or placebo (n 12) three times a day with meals for 10 d. Preheparin LPL and HTGL activities and LPL speci®c activity were measured in the fasted state on days 1, 5, and 10. On days 5 and 10 the study medication (orlistat or placebo) was taken at the beginning of a fat-rich breakfast and serum lipid and lipoprotein levels monitored for 12 h postprandially. On day 10, 15 min postheparin HTGL activity was measured 8 h after the fat-rich breakfast. RESULTS: No differences were found between groups in fasting levels of preheparin LPL or HTGL activity or in LPLspeci®c activity on days 1, 5 and 10. No difference was found between the two treatment groups in postheparin HTGL activity 8 h after the fat-rich breakfast. Also, no differences were found between the two groups in plasma triglycerides or lipoproteins. CONCLUSION: The results indicate that the oral administration of orlistat (120 mg t.i.d.) does not signi®cantly alter plasma triglycerides or lipoproteins, and that the inhibitory effect of orlistat on lipases is limited to the gastrointestinal tract and is not manifested systemically.