Table Of ContentANIMAL 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.
