Impact of weight loss on the metabolic syndrome.

OBJECTIVE: To evaluate the effects of weight loss on the risk of having metabolic syndrome after 1 year of treatment with lifestyle modification alone, pharmacotherapy alone (sibutramine) or the combination of the two. DESIGN: Randomized, controlled, 1-year clinical trial. PATIENTS: One hundred and eighty women and 44 men, 18-65 years of age, with a body mass index of 30-45 kg/m(2), free of uncontrolled hypertension or type 1 or 2 diabetes. INTERVENTION: Fifteen milligrams of sibutramine per day alone, lifestyle modification counseling alone, sibutramine plus lifestyle modification counseling or sibutramine plus brief lifestyle modification counseling. MEASUREMENTS: The metabolic syndrome, as defined by the Adult Treatment Panel III. RESULTS: Before treatment, 34.8% of the participants had the metabolic syndrome. Metabolic syndrome was more prevalent in Caucasians than African Americans (42.5 vs 20.3%; P<0.03), in males than females (65.1 vs 34.9%; P<0.002) and in older (>44 years) than younger (

Effects of glucoprivation on gastric motility and pituitary oxytocin secretion in rats.

Pharmacological doses of insulin (3-25 U/kg sc) elicited feeding and increased gastric motility in rats. In contrast, the glucose analogue 2-deoxy-D-glucose (2-DG), given ip in doses known to increase food intake, had dose-dependent effects on gastric motility: 100 and 200 mg/kg 2-DG increased gastric motility, whereas 500 mg/kg 2-DG virtually eliminated gastric contractions. This latter result resembled the known effects on gastric motility of cholecystokinin (CCK) and LiCl. Moreover, like CCK and LiCl, 500 mg/kg 2-DG stimulated pituitary oxytocin (OT) secretion, and its effects on gastric motility and OT secretion were potentiated by pretreatment with the opioid antagonist naloxone. In contrast, OT secretion was not affected by insulin-induced hypoglycemia with or without naloxone pretreatment. These results suggest that there are two components to the effects of 2-DG on gastric motility: an insulin-like excitatory component and a CCK-LiCl-like inhibitory component. The latter inhibitory component may be mediated by the paraventricular nucleus of the hypothalamus, which has already been implicated in the inhibitory control of gastric motility.