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      Dynamic Responses to Leptin Secretagogues in Lean, Obese, and Massively Obese Men and Women

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          Abstract

          Background/Aim: Basal plasma leptin levels are higher in women than in men and also higher in obese than in lean subjects, but the dynamic leptin secretion has not been well studied. We tested whether the leptin secretory response to glucocorticoid or insulin differs by gender and adiposity status. Methods: Seventy-nine nondiabetic adults, comprising lean [body mass index (BMI; kg/m<sup>2</sup>) ≤25; n = 27], obese (BMI 30–40; n = 28), and massively obese (BMI >40; n = 24) subjects, participated in two separate studies. In study 1, the subjects received oral dexamethasone (4 mg), with blood sampling before and 8 and 16 h after ingestion. In study 2, the subjects underwent a two-step hyperinsulinemic (1.0 mU·kg<sup>–1</sup>/min for 3 h, then 2.0 mU·kg<sup>–1</sup>/min for 3 h), euglycemic (∼100 mg/dl) clamp. Blood samples were obtained at baseline and every 20 min during the clamp. Results: Basal and stimulated leptin levels were higher in women than in men, and higher in the obese groups than in lean subjects. The percentage increase above baseline leptin was similar among men and women within each group, but was ∼30% lower in massively obese compared to lean subjects. Conclusion: Leptin secretory responses to glucocorticoid or insulin stimulation are preserved across a broad adiposity range, with higher absolute responses in women than in men.

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          Most cited references 25

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          Changes in energy expenditure resulting from altered body weight.

          No current treatment for obesity reliably sustains weight loss, perhaps because compensatory metabolic processes resist the maintenance of the altered body weight. We examined the effects of experimental perturbations of body weight on energy expenditure to determine whether they lead to metabolic changes and whether obese subjects and those who have never been obese respond similarly. We repeatedly measured 24-hour total energy expenditure, resting and nonresting energy expenditure, and the thermic effect of feeding in 18 obese subjects and 23 subjects who had never been obese. The subjects were studied at their usual body weight and after losing 10 to 20 percent of their body weight by underfeeding or gaining 10 percent by overfeeding. Maintenance of a body weight at a level 10 percent or more below the initial weight was associated with a mean (+/- SD) reduction in total energy expenditure of 6 +/- 3 kcal per kilogram of fat-free mass per day in the subjects who had never been obese (P < 0.001) and 8 +/- 5 kcal per kilogram per day in the obese subjects (P < 0.001). Resting energy expenditure and nonresting energy expenditure each decreased 3 to 4 kcal per kilogram of fat-free mass per day in both groups of subjects. Maintenance of body weight at a level 10 percent above the usual weight was associated with an increase in total energy expenditure of 9 +/- 7 kcal per kilogram of fat-free mass per day in the subjects who had never been obese (P < 0.001) and 8 +/- 4 kcal per kilogram per day in the obese subjects (P < 0.001). The thermic effect of feeding and nonresting energy expenditure increased by approximately 1 to 2 and 8 to 9 kcal per kilogram of fat-free mass per day, respectively, after weight gain. These changes in energy expenditure were not related to the degree of adiposity or the sex of the subjects. Maintenance of a reduced or elevated body weight is associated with compensatory changes in energy expenditure, which oppose the maintenance of a body weight that is different from the usual weight. These compensatory changes may account for the poor long-term efficacy of treatments for obesity.
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            Cerebrospinal fluid leptin levels: relationship to plasma levels and to adiposity in humans.

            The adipocyte hormone, leptin (OB protein), is proposed to be an "adiposity signal" that acts in the brain to lower food intake and adiposity. As plasma leptin levels are elevated in most overweight individuals, obesity may be associated with leptin resistance. To investigate the mechanisms underlying brain leptin uptake and to determine whether reduced uptake may contribute to leptin resistance, we measured immunoreactive leptin levels in plasma and cerebrospinal fluid (CSF) of 53 human subjects. Leptin concentrations in CSF were strongly correlated to the plasma level in a nonlinear manner (r = 0.92; p = 0.0001). Like levels in plasma, CSF leptin levels were correlated to body mass index (r = 0.43; p = 0.001), demonstrating that plasma leptin enters human cerebrospinal fluid in proportion to body adiposity. However, the efficiency of this uptake (measured as the CSF:plasma leptin ratio) was lower among those in the highest as compared with the lowest plasma leptin quintile (5.4-fold difference). We hypothesize that a saturable mechanism mediates CSF leptin transport, and that reduced efficiency of brain leptin delivery among obese individuals with high plasma leptin levels results in apparent leptin resistance.
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              Recombinant Leptin for Weight Loss in Obese and Lean Adults

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                Author and article information

                Journal
                HRE
                Horm Res Paediatr
                10.1159/issn.1663-2818
                Hormone Research in Paediatrics
                S. Karger AG
                1663-2818
                1663-2826
                2008
                September 2008
                29 July 2008
                : 70
                : 3
                : 174-181
                Affiliations
                aDepartment of Medicine and General Clinical Research Center, University of Tennessee Health Science Center, Memphis, Tenn., and bDivision of Endocrinology, Diabetes and Metabolism, Washington University School of Medicine, St. Louis, Mo., USA
                Article
                145018 Horm Res 2008;70:174–181
                10.1159/000145018
                18663318
                © 2008 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 3, Tables: 2, References: 38, Pages: 8
                Categories
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