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Rosenbaum M.,Columbia University | Kissileff H.R.,Columbia University | Kissileff H.R.,St Lukes Roosevelt Hospital Medical Center | Mayer L.E.S.,Columbia University | And 2 more authors.
Brain Research | Year: 2010

Almost anyone who has ever lost weight can attest that it is harder to sustain weight loss than to lose weight. Maintenance of a 10% or greater reduced body weight is accompanied by decreases in energy expenditure to levels significantly below what is predicted solely on the basis of weight and body composition changes. This disproportionate decline in energy expenditure would not be sufficient to account for the over 80% recidivism rate to pre-weight loss levels of body fatness after otherwise successful weight reduction if there were a corresponding reduction in energy intake. In fact, reduced body weight maintenance is accompanied by increased energy intake above that required to maintain reduced weight. The failure to reduce energy intake in response to decreased energy output reflects decreased satiation and perception of how much food is eaten and multiple changes in neuronal signaling in response to food which conspire with the decline in energy output to keep body energy stores (fat) above a CNS-defined minimum (threshold). Much of this biological opposition to sustained weight loss is mediated by the adipocyte-derived hormone "leptin." © 2010 Elsevier B.V. All rights reserved.


Kissileff H.R.,St Lukes Roosevelt Hospital Medical Center | Kissileff H.R.,Columbia University | Thornton J.C.,St Lukes Roosevelt Hospital Medical Center | Torres M.I.,St Lukes Roosevelt Hospital Medical Center | And 5 more authors.
American Journal of Clinical Nutrition | Year: 2012

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 (W tinitial) 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 W tinitial 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. © 2012 American Society for Nutrition.

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