Gamete and Embryo-fetal Origins of Adult Diseases

228 Pages·2014·2.309 MB·English

by  Ying-Hui Ye, Le-Jun Li, Yue-Zhou Chen (auth.), He-Feng Huang, Jian-Zhong Sheng (eds.)

Gamete and
Embryo-fetal Origins
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He-Feng Huang
Jian-Zhong Sheng
Editors
Gamete and Embryo-fetal Origins
of Adult Diseases

He-Feng Huang (cid:129) Jian-Zhong Sheng
Editors
Gamete and Embryo-fetal
Origins of Adult Diseases
Editors
He-Feng Huang Jian-Zhong Sheng
The Key Laboratory of Reproductive Genetics The Key Laboratory of Reproductive Genetics
Zhejiang University Zhejiang University
Ministry of Education Ministry of Education
Hangzhou Hangzhou
People’s Republic of China People’s Republic of China
Department of Reproductive Endocrinology Department of Pathology and Pathophysiology
Women’s Hospital School of Medicine
School of Medicine Zhejiang University
Zhejiang University Hangzhou
Hangzhou People’s Republic of China
People’s Republic of China
ISBN 978-94-007-7771-2 ISBN 978-94-007-7772-9 (eBook)
DOI 10.1007/978-94-007-7772-9
Springer Dordrecht Heidelberg New York London
Library of Congress Control Number: 2013954520
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Pref ace
Prenatal and early postnatal events increase the risk of some diseases in later life
including diabetes, coronary heart disease and hypertension etc. In 1934, a land-
mark paper, published in the Lancet , found that death rates from all causes in the
UK and Sweden decreased with each successive year-of-birth cohort between 1751
and 1930 [1]. The authors concluded that the health of child is determined by the
environmental conditions existing during early life (0–15 years), and, the health of
the adult is largely determined by the physical constitution of child [1]. In 1977,
Forsdahl discovered a signifi cant positive correlation between infant mortality
rates and later mortality rates from arteriosclerotic heart disease [2]. Poverty in
childhood followed by prosperity in later life is a risk factor for arteriosclerotic
heart disease [2, 3].
Studies in the UK a decade later shifted the focus back to prenatal rather than
postnatal events. In 1989, Barker et al. examined relationships between post-
neonatal mortality for the period 1911–1925 and later adult mortality in 1968–1978.
They found that regional differences in stroke and coronary heart disease mortality
were predicted by birthweight [4]. Barker subsequently showed that lower birth-
weights, and, weight at 1 year, were associated with an increased risk of death from
stroke and coronary heart disease in adults [5]. Barker proposed that the roots of
cardiovascular disease lay in the effects of poverty on the mother, and, undernutrition
in fetal life and early infancy. Subsequent studies in UK, Europe, USA, and China
have confi rmed these fi ndings and shown that it is restricted fetal growth rather than
preterm delivery which carries the risk of later adult diseases [6]. These observations
have been collectively termed the “Barker hypothesis”.
Most human physiological systems and organs begin to develop early in gestation
but become fully mature only after birth. A relatively long gestation and period of
postnatal maturation allows for prolonged pre- and postnatal interactions with the
environment. The primary determinants of fetal growth are genes, the integrity of
the feto-placental unit, and, the appropriate endocrine environment that is largely
represented by insulin action, and, the insulin-like growth factor system [7, 8].
Normal fetal growth and development take place in two phases; the embryonal
and fetal phases: The embryonal phase (1–8 weeks) consists of the proliferation,
organization, and differentiation of the embryo, whereas the fetal phase (9–38
weeks) describes the continued growth and functional maturation of different
v
vi Preface
tissues and organs [7, 8]. Embryonic and fetal periods are clearly vulnerable to
environmental factors, and acquired changes can persist transgenerationally,
despite the lack of continued exposure. One possible explanation is the epigenetic
regulation of the human genome where changes in gene expression or cellular
phenotype result from mechanisms other than changes in the underlying DNA [9].
In 2010, Motrenko proposed the “embryo-fetal origin of diseases” theory, where
proposed abnormal development of gamete and embryo may induce poor health
after birth [10].
Adaptive responses of a gamete or embryo reacting with adverse factors, e.g.
culture systems and manipulations in ART, toxins, endocrine disrupting chemicals,
etc., make it susceptible to permanent damage of organs, congenital abnormality,
and, development of chronic adult diseases. Passing such changes to offspring may
result in transgenerational, epigenetic re-programming with transmission of adverse
traits and characteristics to offspring.
This book systematically introduces the growing body of evidence from epide-
miological observations and clinical and experimental, animal studies that support
the gamete and embryo-fetal origins of the metabolic syndrome.
Hangzhou, People’s Republic of China He-Feng Huang
Hangzhou, People’s Republic of China Jian-Zhong Sheng
References
1. Kermack WO, McKendrick AG, McKinlay PL. Death rates in Great Britain and Sweden: some
general regularities and their signifi cance. Lancet 1934;226:698–703.
2. Forsdahl A. Are poor living conditions in childhood and adolescence an important risk factor
for arteriosclerotic heart disease? Br J Prev Soc Med. 1977;31:91–5.
3. Forsdahl A. Living conditions in childhood and subsequent development of risk factors for
arteriosclerotic heart disease. The cardiovascular survey in Finnmark 1974–75. J Epidemiol
Community Health 1978;32:34–7.
4. Barker DJ, Osmond C, Law CM. The intrauterine and early postnatal origins of cardiovascular
disease and chronic bronchitis. J Epidemiol Community Health 1989;43:237–40.
5. Barker DJ, Winter PD, Osmond C et al. Weight in infancy and death from ischaemic heart
disease. Lancet 1989;2:577–80.
6. Paneth N, Susser M. Early origin of coronary heart disease (the "Barker hypothesis") BMJ
1995;310:411–2.
7. Gluckman PD, Harding JE. Nutritional and hormonal regulation of fetal growth—evolving
concepts. Acta Paediatr. 1994;399: 60–3.
8. Kanaka-Gantenbein Ch, Mastorakos G, Chrousos GP. Endocrine-related causes and conse-
quences of intrauterine growth retardation. Ann NY Acad Sci. 2003;997:150–7.
9. Canani RB, Costanzo MD, Leone L, et al. Epigenetic mechanisms elicited by nutrition in early
life. Nutr Res Rev. 2011;24:198–205.
10. Motrenko T. Embryo-fetal origin of diseases – new approach on epigenetic reprogramming.
Archiv Perinatal Med. 2010;16:11–5.
Contents
1 Physiology of Gametogenesis ..................................................................... 1
Ying-Hui Ye, Le-Jun Li, Yue-Zhou Chen,
He-Feng Huang, and Zhong-Yan Liang
2 Physiology of Embryonic Development ................................................ 39
Ai-Xia Liu, Xin-Mei Liu, Yan-Ling Zhang,
He-Feng Huang, and Chen-Ming Xu
3 Adverse Intrauterine Environment
and Gamete/Embryo-Fetal Origins of Diseases ................................... 61
Min-Yue Dong, Fang-Fang Wang, Jie-Xue Pan,
and He-Feng Huang
4 Gamete/Embryo-Fetal Origins of Diabetes .......................................... 79
He-Feng Huang, Guo-Dian Ding, Shen Tian, and Qiong Luo
5 Gamete/Embryo-Fetal Origins of Cardiovascular Diseases ............... 95
Jian-Zhong Sheng, Li Zhang, Gu-Feng Xu, and Ying Jiang
6 Gamete/Embryo-Fetal Origins of Tumours .......................................... 109
Dan Zhang, He-Feng Huang, Feng Zhang,
Run-Ju Zhang, Yang Song, and Jing-Yi Li
7 Gamete/Embryo-Fetal Origins of Obesity ............................................ 137
He-Feng Huang, Min Jin, and Xian-Hua Lin
8 Gamete/Embryo-Fetal Origins of Mental Disorders ........................... 157
Fan Qu, Lu-Ting Chen, Hong-Jie Pan, and He-Feng Huang
9 Gamete/Embryo-Fetal Origins of Infertility ........................................ 173
Xiao-Ming Zhu, Yu Zhang, Xi-Jing Chen,
and He-Feng Huang
vii
viii Contents
10 Assisted Reproductive Technology
and Gamete/Embryo-Fetal Origins of Diseases ................................... 197
Yi-Min Zhu, Xiao-Ling Hu, Yan-Ting Wu,
Chun Feng, and He-Feng Huang
Index ................................................................................................................. 221
All Contr ibutors
Chen, Lu-Ting M.D., Pan, Jie-Xue M.D.,
Chen, Xi-Jing Ph.D., Qu, Fan Ph.D.,
Chen, Yue-Zhou Ph.D., Sheng, Jian-Zhong Ph.D.,
Ding, Guo-Lian Ph.D., Song, Yang M.D.,
Dong, Min-Yue Ph.D., Tian, Shen M.D.,
Feng, Chun Ph.D., Wang, Fang-Fang Ph.D.,
Hu, Xiao-Ling M.D., Wu, Yan-Ting Ph.D.,
Huang, He-Feng M.D., Xu, Chen-Ming Ph.D.,
Jiang, Ying M.D., Xu, Gu-Feng Ph.D.,
Jin, Min Ph.D., Ye, Ying-Hui Ph.D.,
Li, Jing-Yi M.D., Zhang, Dan Ph.D.,
Li, Le-Jun M.D., Zhang, Feng Ph.D.,
Liang, Zhong-Yan Ph.D. Zhang, Li Ph.D.,
Lin, Xian-Hua M.D., Zhang, Run-Ju Ph.D.,
Liu, Ai-Xia Ph.D., Zhang, Yan-Ling Ph.D.,
Liu, Xin-Mei Ph.D., Zhang, Yu Ph.D.,
Luo, Qiong Ph.D., Zhu, Xiao-Ming Ph.D.,
Pan, Hong-Jie M.D., Zhu, Yi-Min Ph.D.,
ix