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Vol. 68, Suppl. 5, 2007
Issue release date: December 2007
Section title: Combined Plenary Lecture 2
Horm Res 2007;68:5–7
(DOI:10.1159/000110462)

Insights from the Genetics of Severe Childhood Obesity

Farooqi S.
Department of Medicine, Addenbrooke’s Hospital, University of Cambridge, Cambridge, UK

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Article / Publication Details

First-Page Preview
Abstract of Combined Plenary Lecture 2

Published online: 12/10/2007

Number of Print Pages: 3
Number of Figures: 0
Number of Tables: 0

ISSN: 1663-2818 (Print)
eISSN: 1663-2826 (Online)

For additional information: http://www.karger.com/HRP

Abstract

Background: The identification and characterization of monogenic obesity syndromes have improved our understanding of the inherited component of severe obesity and have had undoubted medical benefits. This knowledge has also helped to dispel the notion that obesity represents an individual defect in behaviour with no biological basis. Conclusions: For individuals at highest risk for complications of severe obesity, such findings provide a starting point for providing more rational mechanism-based therapies, as has successfully been achieved for congenital leptin deficiency.


Article / Publication Details

First-Page Preview
Abstract of Combined Plenary Lecture 2

Published online: 12/10/2007

Number of Print Pages: 3
Number of Figures: 0
Number of Tables: 0

ISSN: 1663-2818 (Print)
eISSN: 1663-2826 (Online)

For additional information: http://www.karger.com/HRP


Copyright / Drug Dosage

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 or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
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 goverment 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.

References

  1. Kopelman PG: Obesity as a medical problem. Nature 2000;404:635–643.
  2. Farooqi IS: Genetic and hereditary aspects of childhood obesity. Best Pract Res Clin Endocrinol Metab 2005;19:359–374.
  3. Barsh GS, Farooqi IS, O’Rahilly S: Genetics of body-weight regulation. Nature 2000;404:644–651.
  4. Maes HH, Neale MC, Eaves LJ: Genetic and environmental factors in relative body weight and human adiposity. Behav Genet 1997;27:325–351.
  5. Friedman JM, Halaas JL: Leptin and the regulation of body weight in mammals. Nature 1998;395:763–770.
  6. Schwartz MW, Woods SC, Porte D Jr, Seeley RJ, Baskin DG: Central nervous system control of food intake. Nature 2000;404:661–671.
  7. Coll AP, Farooqi IS, Challis BG, Yeo GS, O’Rahilly S: Proopiomelanocortin and energy balance: insights from human and murine genetics. J Clin Endocrinol Metab 2004;89:2557–2562.
  8. Zigman JM, Elmquist JK: Minireview: From anorexia to obesity – the yin and yang of body weight control. Endocrinology 2003;144:3749–3756.
  9. Montague CT, Farooqi IS, Whitehead JP, et al: Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature 1997;387:903–908.
  10. Farooqi IS, Matarese G, Lord GM, et al: Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency. J Clin Invest 2002;110:1093–1103.
  11. Ozata M, Ozdemir IC, Licinio J: Human leptin deficiency caused by a missense mutation: multiple endocrine defects, decreased sympathetic tone, and immune system dysfunction indicate new targets for leptin action, greater central than peripheral resistance to the effects of leptin, and spontaneous correction of leptin-mediated defects. J Clin Endocrinol Metab 1999;84:3686–3695.
  12. Farooqi IS, Jebb SA, Langmack G, et al: Effects of recombinant leptin therapy in a child with congenital leptin deficiency. N Engl J Med 1999;341:879–884.
  13. Farooqi IS, Wangensteen T, Collins S, et al: Clinical and molecular genetic spectrum of congenital deficiency of the leptin receptor. N Engl J Med 2007;356:237–247.
  14. Krude H, Biebermann H, Luck W, Horn R, Brabant G, Gruters A: Severe early-onset obesity, adrenal insufficiency and red hair pigmentation caused by POMC mutations in humans. Nat Genet 1998;19:155–157.
  15. Farooqi IS, Drop S, Clements A, et al: Heterozygosity for a POMC-null mutation and increased obesity risk in humans. Diabetes 2006;55:2549–2553.
  16. Challis BG, Pritchard LE, Creemers JW, et al: A missense mutation disrupting a dibasic prohormone processing site in pro-opiomelanocortin (POMC) increases susceptibility to early-onset obesity through a novel molecular mechanism. Hum Mol Genet 2002;11:1997–2004.
  17. Lee YS, Challis BG, Thompson DA, et al: A POMC variant implicates beta-melanocyte-stimulating hormone in the control of human energy balance. Cell Metab 2006;3:135–140.

    External Resources

  18. Vaisse C, Clement K, Guy-Grand B, Froguel P: A frameshift mutation in human MC4R is associated with a dominant form of obesity [letter]. Nat Genet 1998;20:113–114.
  19. Yeo GS, Farooqi IS, Aminian S, Halsall DJ, Stanhope RG, O’Rahilly S: A frameshift mutation in MC4R associated with dominantly inherited human obesity [letter]. Nat Genet 1998;20:111–112.
  20. Farooqi IS, Keogh JM, Yeo GS, Lank EJ, Cheetham T, O’Rahilly S: Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene. N Engl J Med 2003;348:1085–1095.
  21. Larsen LH, Echwald SM, Sorensen TI, Andersen T, Wulff BS, Pedersen O: Prevalence of mutations and functional analyses of melanocortin 4 receptor variants identified among 750 men with juvenile-onset obesity. J Clin Endocrinol Metab 2005;90:219–224.
  22. Alharbi KK, Spanakis E, Tan K, et al: Prevalence and functionality of paucimorphic and private MC4R mutations in a large, unselected European British population, scanned by melt MADGE. Hum Mutat 2007;28:294–302.
  23. Farooqi IS: The severely obese patient – a genetic work-up. Nat Clin Pract Endocrinol Metab 2006;2:172–177.

    External Resources