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      Coronary Heart Disease: A Disorder of Growth

      Hormone Research in Paediatrics

      S. Karger AG

      Coronary heart disease, Fetal and childhood growth, Developmental plasticity

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          Abstract

          A new ‘developmental’ model for the origins of coronary heart disease and the related disorders of type 2 diabetes, hypertension and stroke is emerging. The finding that people who develop these disorders have altered growth in utero, during infancy and childhood provides a new starting point for research. The immediate prospect for prevention is through protecting infant growth and preventing accelerated weight gain in children made vulnerable to later disease by small size at birth and during infancy. Ultimately we need to optimize maternal diet and composition before and during pregnancy. Despite current levels of nutrition in Western countries the nutrition of many fetuses and infants remains suboptimal because the nutrients available are unbalanced or because their delivery is constrained by the long and vulnerable fetal supply line.

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          Most cited references 4

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          Role of fetal and infant growth in programming metabolism in later life.

           C. Hales,  Tanay Desai (1997)
          Fetal growth and development is dependent upon the nutritional, hormonal and metabolic environment provided by the mother. Any disturbance in this environment can modify early fetal development with possible long-term outcomes as demonstrated by extensive work on 'programming'. Growth restriction resulting from a deficit in tissue/organ cell number (as measured by tissue DNA content) is irrecoverable. However, when the cell size (or cell protein content) is reduced, the effects on growth may not be permanent. Recent epidemiological studies using archival records of anthropometric measurements related to early growth in humans have shown strong statistical associations between these indices of early development and diseases in later life. It has been hypothesised that the processes explaining these associations involve adaptive changes in fetal organ development in response to maternal and fetal malnutrition. These adaptations may permanently alter adult metabolism in a way which is beneficial to survival under continued conditions of malnutrition but detrimental when nutrition is abundant. This hypothesis is being tested in a rat model which involves studying the growth and metabolism in the offspring of rat dams fed a low-protein diet during pregnancy and/or lactation. Using this rat model, it has been demonstrated that there is: (i) Permanent growth retardation in offspring nursed by dams fed a low-protein diet. (ii) Permanent and selective changes in organ growth. Essential organs like the brain and lungs are relatively protected from reduction in growth at the expense of visceral organs such as the liver, pancreas, muscle and spleen. (iii) Programming of liver metabolism as reflected by permanent changes in activities of key hepatic enzymes of glycolysis and gluconeogenesis (glucokinase and phosphoenolpyruvate carboxykinase) in a direction which would potentially bias the liver towards a 'starved' setting. We have speculated that these changes could be a result of altered periportal and perivenous regions of the liver which may also affect other aspects of hepatic function. (iv) Deterioration in glucose tolerance with age. (v) An increase in the life span of offspring exposed to maternal protein restriction only during the lactation period, and a decrease in life span when exposed to maternal protein restriction only during gestation. These studies show that hepatic metabolism and even longevity can be programmed by events during early life.
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            Metabolic zonation of the liver: Regulation and implications for liver function

             Rolf Gebhardt (1992)
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              • Abstract: not found
              • Article: not found

              Fetal growth and coronary heart disease in South India

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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
                978-3-8055-7539-3
                978-3-318-00942-2
                1663-2818
                1663-2826
                2003
                January 2003
                17 November 2004
                : 59
                : Suppl 1
                : 35-41
                Affiliations
                MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, UK
                Article
                67843 Horm Res 2003;59(suppl 1):35–41
                10.1159/000067843
                12566719
                © 2003 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: 2, Tables: 4, References: 49, Pages: 7
                Categories
                The Neonate and Endocrine Disease

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