ABSTRACT
BACKGROUND: Individuals who are weight-reduced or leptin deficient have a lower energy expenditure coupled with higher hunger and disinhibition and/or delayed satiation compared with never-weight-reduced control subjects. Because exogenous leptin inhibits feeding in congenitally leptin-deficient humans, reduced leptin signaling may reduce the expression of feeding inhibition in humans. OBJECTIVE: The objective was to test the hypothesis that reduced leptin signaling may reduce the expression of feeding inhibition (ie, blunt satiation) in humans by examining the effects of leptin repletion on feeding behavior after weight loss. DESIGN: Ten obese humans (4 men, 6 women) were studied as inpatients while they received a weight-maintaining liquid-formula diet. Satiation was studied by measuring intake and ratings of appetite-related dispositions 3 h after ingestion of 300 kcal of the liquid-formula diet. The subjects were studied at each of 3 time periods: 1) while they maintained their usual weight (Wt(initial)) and then after weight reduction and stabilization at 10% below initial weight and while they received 5 wk of either 2) twice-daily injections of placebo (Wt(-10%placebo)) or 3) "replacement doses" of leptin (Wt(-10%leptin)) in a single-blind crossover design with a 2-wk washout period between treatments. Energy expenditure was also measured at each study period. RESULTS: Both energy expenditure and visual analog scale ratings that reflect satiation were significantly lower at Wt(-10%placebo) than at Wt(initial) and Wt(-10%leptin). CONCLUSION: The results are consistent with the hypothesis that the absence of leptin signaling after weight loss may blunt the expression of feeding inhibition in humans.
Subject(s)
Appetite/physiology , Energy Metabolism/physiology , Leptin/metabolism , Obesity/physiopathology , Satiation/physiology , Weight Loss/physiology , Adult , Appetite/drug effects , Cross-Over Studies , Diet, Reducing , Energy Metabolism/drug effects , Female , Humans , Leptin/pharmacology , Male , Obesity/diet therapy , Obesity/metabolism , Satiation/drug effects , Single-Blind MethodABSTRACT
Bulimia Nervosa (BN) is an eating disorder characterized by recurrent episodes of binge eating. During binge eating episodes, patients often describe the rapid consumption of food, and laboratory studies have shown that during binges patients with BN eat faster than normal controls (NC), but the hypothesis that a rapid rate of eating contributes to the excessive intake of binge meals has not yet been experimentally tested. The aim of this study was to assess the effect of eating rate on binge size in BN, in order to determine whether binge size is mediated, in part, by rate of eating. Thirteen BN and 14 NC subjects were asked to binge eat a yogurt shake that was served at a fast rate (140 g/min) on one occasion and at a slow rate (70 g/min) on another. NC subjects consumed 169 g more when eating at the fast rate than when eating at the slow rate. In contrast, consumption rates failed to influence binge size in patients with BN (fast: 1205 g; slow: 1195 g). Consequently, there was a significant group by rate interaction. As expected, patients with BN consumed more overall than NC subjects (1200 g vs. 740 g). When instructed to binge in the eating laboratory, patients with BN ate equally large amounts of food at a slow rate as at a fast rate. NC subjects ate less at a slow rate. These findings indicate that in a structured laboratory meal paradigm binge size is not affected by rate of eating.
