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      Relationship between Changes in Plasma Leptin Concentrations and Plasminogen Activator Inhibitor-1 in Obese Prepubertal Children after Nine Months of Treatment

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          Abstract

          Background/Aims: The metabolic syndrome (MS) is associated with insulin resistance (IR), inappropriate fibrinolysis and high plasma leptin concentrations. The aim of this study was to quantify fibrinolysis and MS-related variables in obese prepubertal children and to evaluate changes in these variables as a result of improved body mass index (BMI), IR and leptin levels following 9 months of treatment. Methods: The homeostasis model assessment for insulin resistance (HOMA-IR), leptin, plasminogen activator inhibitor-1 (PAI-1) and lipid profile were studied at baseline in obese (n = 50) and nonobese children (n = 50), and after 9 months of treatment in obese children. Results: In the cross-sectional study the mean values for insulin, HOMA-IR, triglycerides, leptin and PAI-1 were significantly higher in obese children than in controls. High-density lipoprotein cholesterol (HDLc) and apolipoprotein A-1 were significantly lower. In the longitudinal study, after 9 months, children with lowered BMI standard deviation score displayed a significant decrease in insulin, HOMA-IR, PAI-1, leptin and triglyceride levels, and an increase in HDLc. Only leptin proved to be an independent predictive factor for changes in PAI-1 (p = 0.010). Conclusion: Obesity-linked disorders appear in obese children prior to puberty; these disorders can be improved by decreasing BMI. Changes in leptin levels were found to independently predict changes in PAI-1 in obese children and can help to diagnose complications associated with the obesity.

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          Most cited references29

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          Leptin and atherosclerosis.

          Leptin, a 167-amino acid peptide hormone produced by white adipose tissue, is primarily involved in the regulation of food intake and energy expenditure. Leptin receptors are expressed in many tissues including the cardiovascular system. Plasma leptin concentration is proportional to body adiposity and is markedly increased in obese individuals. Recent studies suggest that hyperleptinemia may play an important role in obesity-associated cardiovascular diseases including atherosclerosis. Leptin exerts many potentially atherogenic effects such as induction of endothelial dysfunction, stimulation of inflammatory reaction, oxidative stress, decrease in paraoxonase activity, platelet aggregation, migration, hypertrophy and proliferation of vascular smooth muscle cells. Leptin-deficient and leptin receptor-deficient mice are protected from arterial thrombosis and neointimal hyperplasia in response to arterial wall injury. Several clinical studies have demonstrated that high leptin level predicts acute cardiovascular events, restenosis after coronary angioplasty, and cerebral stroke independently of traditional risk factors. In addition, plasma leptin correlates with markers of subclinical atherosclerosis such as carotid artery intima-media thickness and coronary artery calcifications. Inhibition of leptin signaling may be a promising strategy to slow the progression of atherosclerosis in hyperleptinemic obese subjects.
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            Changes in the atherogenic risk factor profile according to degree of weight loss.

            The atherogenic risk factor profile in obese subjects is characterised by hypertension, reduced high density lipoprotein (HDL) cholesterol, increased low density lipoprotein (LDL) cholesterol and triglycerides, and insulin resistance. To examine the amount of weight reduction required to improve the atherogenic profile. Changes of systolic and diastolic blood pressure, HDL and LDL cholesterol, triglycerides, and insulin resistance, based on the HOMA model over a one year period were studied in obese children, who attended the intervention programme "Obeldicks". The children were divided into four groups according to the change in body mass index standard deviation score (SDS-BMI): group I, increase in SDS-BMI; group II, decrease in SDS-BMI or =0.25- or =0.5. A total of 130 children (mean age 10.7 years, range 4-15; mean SDS-BMI 2.5, range 2.0-4.0) were studied. The four groups did not differ in age, gender, or degree of overweight (SDS-BMI). An increasing SDS-BMI (group I: n = 20) was followed by a significant increase in insulin resistance (HOMA). Systolic and diastolic blood pressure, LDL cholesterol, triglycerides, and insulin resistance (HOMA) decreased significantly while HDL cholesterol increased significantly in group IV (n = 37). LDL cholesterol also decreased significantly in group III (n = 40); there was no significant change of the other parameters in groups I, II, and III. Over a time period of one year increasing weight in obese children leads to an increase in insulin resistance. Weight loss is associated with an improvement in the atherogenic profile and in insulin resistance, but only if the SDS-BMI decreases by at least 0.5 over a one year period.
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              Plasminogen activator inhibitor-1, inflammation, obesity, insulin resistance and vascular risk.

              Elevated plasma plasminogen activator inhibitor-1 (PAI-1) level is a core feature of insulin-resistance syndrome (IRS). Atherothrombotic complications in IRS are partly attributed to impaired fibrinolysis caused by increased plasma PAI-1 levels. Although the etiology of IRS is far from being explained, the clustering of inflammation, adipose tissue accumulation and insulin resistance suggests an etiopathological link. Proinflammatory cytokines might regulate PAI-1 expression in IRS; however, more studies are needed to confirm this complex mechanism in humans. Furthermore, modifying PAI-1 expression by PAI-1 inhibitors provides a new challenge and may reveal the true role of PAI-1 in atherosclerotic and insulin resistance processes.
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                Author and article information

                Journal
                ANM
                Ann Nutr Metab
                10.1159/issn.0250-6807
                Annals of Nutrition and Metabolism
                S. Karger AG
                0250-6807
                1421-9697
                2013
                December 2013
                15 October 2013
                : 63
                : 3
                : 216-222
                Affiliations
                aClinical Laboratory Department, Valle de los Pedroches Hospital, and bHealth Center of Pozoblanco, Pozoblanco, cSchool of Medicine and dGrupo PAIDI CTS-329 (IMIBIC), Universidad de Córdoba, and ePediatric Department, Reina Sofía Hospital, Córdoba, Spain
                Author notes
                *Dr. Miguel Valle Jiménez, Clinical Laboratory Department, Valle de los Pedroches Hospital, C/Juan del Rey Calero s/n, ES-14400 Pozoblanco, Córdoba (Spain), E-Mail vallej90@yahoo.es
                Article
                351597 Ann Nutr Metab 2013;63:216-222
                10.1159/000351597
                24135306
                e835dbca-f794-490e-82e4-22427b57b6ea
                © 2013 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.

                History
                : 19 March 2012
                : 18 April 2013
                Page count
                Figures: 1, Tables: 5, Pages: 7
                Categories
                Original Paper

                Nutrition & Dietetics,Health & Social care,Public health
                Children,Leptin,Insulin resistance,Obesity,Metabolic syndrome,Plasminogen activator inhibitor-1

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