Animal Models — Disorders of Eating Behaviour and Body Composition PDF
Preview Animal Models — Disorders of Eating Behaviour and Body Composition
ANIMAL MODELS - DISORDERS OF EATING BEHAVIOUR AND BODY COMPOSITION ANIMAL MODELS - DISORDERS OF EATING BEHAVIOUR AND BODY COMPOSITION edited by John B. Owen University of Wales, Bangor, UK and Janet L. Treasure and David A. Collier Institute of Psychiatry, University of London, UK Springer-Science+ Business Media, B. V A C.lP. Catalogue record for this book is available from the Library of Congress. ISBN 978-90-481-5743-3 ISBN 978-94-015-9662-6 (eBook) DOI 10.1007/978-94-015-9662-6 Printed on acid-free paper All Rights Reserved © 2001 Springer Science+Business Media Dordrecht Originally published by Kluwer Academic Publishers, Bosyon in 2001. Softcover reprint of the hardcover 1s t edition 2001 No part of the material protected by this copyright notice may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording or by any information storage and retrieval system, without written permission from the copyright owner. Contents Introduction vii Part 1 Human disorders of eating behaviour and body composition Chapter 1 Obesity syndromes 1 M S Bray, D B Allison Chapter 2 Tlhe spectrum of eating disorders in humans 19 J L Treasure, D A Collier Chapter 3 Free-choice diet selection - the economics of eating 51 C V Phillips Part 2 Diet selection and aberrations of body composition Chapter 4 Diet selection in wild animals 69 LHansson Chapter 5 The animal within: lessons from the feeding behaviour of farm animals 83 Kyriazakis Chapter 6 Exercise and diet-induced obesity in mice 97 RRBell Part 3 Genetic models of animal obesity Chapter 7 The obesity (ob) gene and leptin in animal models of obesity 119 K A Augustine-Rauch Chapter 8 Genetic susceptibility of rodents to diet-induced 133 obesity J Harrold Part 4 Genetic susceptibility to leanness in animals Chapter 9 Muscle enhanced traits in cattle and sheep 159 N E Cockett, C A Bidwell v vi Chapter 10 The halothane gene and leanness and stress susceptibility in pigs 173 P Kathirvel, A L Archibald Part 5 Anorexia models Chapter 11 The Anorexia Mouse 193 J Johansen, M Schalling Chapter 12 Anorexia-like wasting syndromes in pigs 205 S C Kyriakis Chapter 13 Laboratory animal models for investigating the mechanisms and function of parasite-induced anorexia 223 J G Mercer, L H Chappell Conclusion Implications for understanding and treating human eating disorders 243 Editorial Index 247 Introduction The book aims to review knowledge on the disorders of eating behaviour and body composition in some of the non-primate higher animals and to relate these to similar conditions in humans. With advances in understanding the nature of these disorders and their biological basis, it seems timely to assess what cross-species comparisons can tell us about the general underlying factors at work. This may also help to delineate what may be a general biological basis that humans share with their higher animal comrade species and what may distinguish human from non-human, particularly in a cultural context. This could help in combating better the problems of these conditions in the animal species as well as in man and in suggesting well-based preventive measures. As far as people are concerned the last two decades of the 20th century have shown a significant increase in obesity in the richer countries, particularly the USA (Table 1). Possibly associated with the obesity boom, there is an increasing awareness of other disorders of eating behaviour and body composition. These range from anorexia nervosa, at the other end of body composition to obesity, to others, such as bulimia, with more variable effects on body composition. It has been apparent for some time that the recent marked change in human body condition, estimated by Body Mass Index (BMI), was not a uniform occurrence over the whole range of BM!. Although the mean value for the populations concerned was increasing there was an even more marked increase in the variance of BMI, indicating that the distribution of BMI was changing. Flegal and Troiano (2000) have studied the distribution of BMI in the US population, recorded in the third National Health and Nutrition Examination Survey (NHANES III: 1988-94) and compared it with values from earlier comparable surveys. These were carried out for adults from 1976-1980 and for children and adolescents from 1963-1970. These data are the most comprehensive available and relate to possibly the extreme in terms of the country trends that have been examined, although other countries are fast following in the same direction. The increase in mean values of BMI between the earlier and latest surveys are shown in Table 1 These results show that for children and young people, including men up to 50 years old, the BMI values for at least the lower half of the distribution have remained remarkably constant. On the other hand the frequencies in almost all the sex/age categories have shown marked progressive increases in the upper part of the BMI distribution. Also for men in the 50+ age groups and all adult females (20+ y), except perhaps the oldest female category (70-74 y of age), there is in addition to the marked increase in frequency at the upper end of the distribution, a modest increase in BMI in the lower part of the distribution. vii viii Table 1 Trends in mean BMI values in the USA Prevalence of Mean BMI obesitv (BMI;:::30) NHANES NHANES Age-sex II III 11 III Men 20-29y 24.3 25.2 8.1 12.5 30-39y 25.6 26.5 11.9 17.2 40-49y 26.4 27.3 15.4 23.1 50-59y 26.2 27.8 14.1 28.9 60-69y 25.7 27.4 13.5 24.8 70-74y 25.4 26.8 13.4 21.1 Women 20-29y 23.1 24.3 8.9 14.6 30-39y 24.9 26.3 16.8 25.8 40-49y 25.7 27.0 18.1 26.9 50-59y 26.5 28.4 22.4 35.6 60-69y 26.5 27.6 22.0 29.8 70-74y 26.5 27.3 18.4 25.7 There are therefore two clear components to the trend in the increased mean BMI value of the subgroups within this population. Firstly there appears to be an underlying general increase in body condition, apparent over the whole range of BMI, noticeable only in the adult women and the older male age groups. Then there is the dramatic increase in the frequencies at the upper end of the BMI distribution, noticeable in practically all age/sex groups. This progressive increase in the population proportion at the higher BMI categories, since 1980, suggests that changes in environmental factors are involved. Of these, diet composition and level of body activity have been seen as prime causal factors. Both these factors, commonly manifest as greed and sloth, have well-known voluntary choice elements in their involvement. The suggestion of a progressive environmental causation at first sight may seem to play down the possible role of genetic factors in both eating disorders and obesity. However it is increasingly evident that there is a multifactorial causality, including the role of the environment, in uncovering thresholds of genetic susceptibility to extreme manifestations of these disorders, possibly influenced by relatively few genes. In addition there is the less pronounced progressive weight increases in some age/sex groups, over the whole range of body composition, which may indicate a more direct environmental influence. Correspondingly trends in anorexia/weight-loss not only encompass tendencies to extremes of normal leanness but also genetic susceptibility to catastrophic breakdown in eating behaviour and resultant life threatening emaciation. This lower end of the BMI range cannot be so clearly delineated as the upper, obese, end in these population statistics. ix This is due to the low frequency of true anorexia nervosa as compared with obesity and the variable effect of the other eating disorders, on BM!. The lack of clear understanding and delineation of the complex factors involved has undoubtedly contributed to the poor outcome of treatment and prevention measures over the whole range of these disorders, despite the enormous expenditure on them in the Western world. The cost of these disorders in terms of human health is very high. The misery and morbidity of eating disorders are well known. Indirectly obesity can be debilitating and lead to many other serious health problems such as heart disease. Ironically our closest non-human partners, domestic pets, are also becoming prone to obesity problems. It therefore seems important to see whether knowledge about these conditions and their causation in animal models could be a valuable asset in understanding human disorders. Observations on animals include a variety of possible relevant information, ranging from studies of diet selection in wild animals to observations and experiments on domesticated (including laboratory) animals. The use of experiments must however be delicately balanced between the need to provide positive benefits in combating difficult and sometimes intractable disorders of humans and domesticated animals and the effect on the welfare the experimental animals themselves. This is in addition to the care necessary to ensure that observations on animal models are not wrongly interpreted and applied to human therapy. The book aims to survey some of the wealth of knowledge that is accumulating on appetite control, feeding behaviour and breakdowns in these mechanisms, resulting in a range of syndromes of obesity and emaciation, in wild and domesticated animals. These studies impinge on the general knowledge of the control mechanisms that may be common to all higher animals and are underlain by a complex genetic network. These observations can add to and enrich the store of knowledge on human subjects and provide clues for furthur research with human subjects such as that on possible underlying candidate genes. These animal studies are even more important with the rapid disappearance of, and the paucity of archeological evidence about, the eating behaviour and body composition of anything resembling primitive hunter/gathering societies. Much of modern man's evolutionary development occurred during the operation of these primitive social structures and eating habits. Modern disorders may therefore be the consequence of recent departure, particularly in the last half-century, from more traditional lifestyles, to which Homo sapiens has not yet adapted. Reference Flegal KM, Troiana RP. Changes in the distribution of body mass index of adults and children in the US popUlation. In! J Obesity 2000; 24: 807-18. PARTl Human disorders of eating behaviour and body composition Chapter 1 OBESITY SYNDROMES Molly S. Bray Human Genetics Center University of Texas Health Science Center at Houston David B. Allison Obesity Research Center St. Luke'slRoosevelt Hospital & Institute for Human Nutrition Columbia University College ofP hysicians & Surgeons ABSTRACT In this chapter we describe a variety of syndromic obesities. These are distinct obesities characterized by a specific phenotypic pattern and in many cases a single specific genetic cause. In some cases, the specific genes involved have been discovered and provide insights into both potential treatments for afflicted individuals and the mechanisms which underlie body weight regulation. The known obesity syndromes include dominant and recessive modes of inheritance, polygenic obesities and imprinted genetic transmission. Comparisons between selected animal modes of obesity and human obesity syndromes are presented. These comparisons illustrate the important cross-species effects of certain genes, point out potential candidate genes with as yet undemonstrated roles in human obesity, and highlight possible physiological pathways for further investigation in human obesity studies. INTRODUCTION A syndrome can be defined as a group of signs or symptoms that collectively characterize a disease or abnormal condition. To date, a number of syndromes have been identified in which obesity is a partial, if not primary, defect in the affected individual. These obesity syndromes may be the consequence of a defect in a single gene, defects in multiple genes, or may result from the complex interaction of multiple environmental, and genetic factors. Many obesity syndromes such as Prader-Willi syndrome, Bardet- J.B. Owen et al. (eels.), Animal Models - Disorders ofE ating Behaviour and Body Composition, 1-18. © 2001 Kluwer Acodemic Publishers.
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