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Managing the Prenatal Environment to Enhance Livestock Productivity

:	Paul L. Greenwood, Alan W. Bell, Philip E. Vercoe, Gerrit J. Viljoen
:	Paul L. Greenwood, Alan W. Bell, Philip E. Vercoe, Gerrit J. Viljoen
:	Managing the Prenatal Environment to Enhance Livestock Productivity
:	Springer-Verlag
:	9789048131358
:	1
:	CHF 134.60
:

:	Zoologie
:	English

:	298
:	Wasserzeichen/DRM
:	PC/MAC/eReader/Tablet
:	PDF

Prenatal life is the period of maximal development in animals, and it is well recognised that factors that alter development can have profound effects on the embryonic, fetal and postnatal animal. Scientists involved in research on livestock productivity have for decades studied postnatal consequences of fetal development on productivity. Recently, however, there has been a surge in interest in how to manage prenatal development to enhance livestock health and productivity. This has occurred largely due to the studies that show human health in later life can be influenced by events during prenatal life, and establishment of the Fetal Origins and the Thrifty Phenotype Hypotheses. This book, Managing the Prenatal Environment to Enhance Livestock Productivity reviews phenotypic consequences of prenatal development, and provides details of mechanisms that underpin these effects in ruminants, pigs and poultry. The chapters have been divided into three parts: Quantification of prenatal effects on postnatal productivity, mechanistic bases of postnatal consequences of prenatal development and regulators of fetal and neonatal nutrient supply.

Managing the Prenatal Environment to Enhance Livestock Productivity is a reference from which future research to improve the level of understanding and capacity to enhance productivity, health and efficiency of livestock in developing and developed countries will evolve. It is particularly timely given the development of molecular technologies that are providing new insight into regulation and consequences of growth and development of the embryo, fetus and neonate.

"Chapter 4 Biological Mechanisms of Fetal Development Relating to Postnatal Growth, Efficiency and Carcass Characteristics in Ruminants (p. 93-94)

John M. Brameld, Paul L. Greenwood, and Alan W. Bell

Introduction

Over recent years there has been a lot of interest in the effects of prenatal environment on subsequent development of tissues and the postnatal consequences. In farm animal species this has particularly related to muscle and fat development and the later consequences in terms of body composition at slaughter. Studies have been carried out in a variety of species, including rats, guinea pigs, pigs, sheep and, more recently, cattle. This chapter will concentrate on the evidence for effects of prenatal environment on development of muscle and adipose cells in ruminant species, the possible mechanisms for these effects and the long-term consequences relating to postnatal growth and body composition.

4.1 Prenatal Development of Carcass Tissues

All tissues within the body develop from the single cell formed when the ovum is fertilised by a sperm. That single cell goes through thousands of cell cycles in order to replicate (proliferate) and form the thousands of cells within each tissue in the developing fetus and resulting offspring. The rates of cell proliferation are dependent upon the balance between factors that stimulate and those that inhibit cell proliferation.

Often those factors are proteins and include hormones (e.g. insulin) and growth factors (e.g. epidermal growth factor (EGF) and platelet derived growth factor (PDGF)). Hence cell proliferation is needed to produce the numbers of cells required to make up a whole organism, but the specialisation of those cells into specific, functional cell types involves the process of cell differentiation. In order for cells to terminally differentiate they must exit the cell cycle and therefore, in general, factors that stimulate proliferation will inhibit differentiation and vice versa.

The majority of differentiated cell types (e.g. hepatocyte, adipocyte and muscle fibre) are therefore unable to proliferate unless they are able to de-differentiate into a precursor cell type. The process of differentiation always involves the switching on of cell- or tissue-specific genes via activation of transcription factors that induce the molecular and morphological changes that result in that cell becoming a specific cell-type. As for proliferation, a variety of factors regulate differentiation, both positively and negatively.

Again various hormones (e.g. insulin, thyroid hormones) and growth factors (e.g. Transforming Growth Factorβ, insulin-like growth factors I and II) are involved, but also some nutrients (e.g. vitamin A), act as ligands for nuclear hormone receptors and thereby regulate gene transcription in a similar manner to transcription factors [111]."

	Preface	5
	Contents	7
	Contributors	9
	Introduction	11
	Part I Quantifying the Magnitude of Prenatal Effects on Productivity	13
	1 Postnatal Consequences of the Maternal Environment and of Growth During Prenatal Life for Productivity of Ruminants	14
	1.1 Introduction	14
	1.1 Managing the Prenatal Environment	15
	1.2 Postnatal Consequences of the Prenatal Environment	15
	1.2.1 Postnatal Growth and Size	16
	1.2.1.1 Studies of Sheep Reared Artificially to Weaning	17
	1.2.1.2 Studies of Sheep Reared to Weaning on Their Dams	18
	1.2.1.3 Studies of Cattle	25
	1.2.2 Nutrient Intake, Digestibility and Efficiency of Nutrient Utilisation	27
	1.2.3 Body and Carcass Composition	30
	1.2.3.1 Sheep	30
	1.2.3.2 Cattle	33
	1.2.4 Meat Quality	34
	1.2.5 Wool Production and Quality	34
	1.2.6 Reproductive Performance	36
	1.2.6.1 Female Reproductive Performance	36
	1.2.6.2 Male Reproductive Performance	38
	1.2.7 Lactational Performance	38
	1.3 Conclusions	38
	References	40
	2 Quantification of Prenatal Effects on Productivity in Pigs	48
	2.1 Introduction	48
	2.1 Litter Variability	49
	2.1.1 Litter Size and Birth Weight	50
	2.1.2 Postnatal Performance	52
	2.1.3 Carcass Composition	54
	2.2 Feeding of the Sow During Gestation	55
	2.2.1 Sow Performance	55
	2.2.1.1 Feed Intake	55
	2.2.1.2 Protein Intake	57
	2.2.1.3 Supplementation with L-Carnitine	58
	2.2.2 Fetal Growth and Birth Weight	59
	2.2.2.1 Feed Intake	59
	2.2.2.2 Protein Intake	60
	2.2.2.3 Supplementation with L-Carnitine	61
	2.2.3 Postnatal Growth	61
	2.2.3.1 Feed Intake	61
	2.2.3.2 Protein Intake	65
	2.2.3.3 Supplementation with L-Carnitine	66
	2.2.4 Carcass Composition	67
	2.2.4.1 Feed Intake	67
	2.2.4.2 Protein Intake	68
	2.3 Sow Porcine Growth Hormone Treatment During Gestation	68
	2.3.1 Sow Performance	69
	2.3.2 Litter Size	72
	2.3.3 Fetal Growth	72
	2.3.4 Postnatal Performance and Carcass Composition	73
	2.4 Summary	74
	2.5 Future Perspectives	76
	References	77
	3 Managing Prenatal Development of Broiler Chickens to Improve Productivity and Thermotolerance	81
	3.1 Introduction	81
	3.1 The Complexity of the Transition from Embryo to Independent Chick	81
	3.2 Feeding the Embryo Before Hatch	84
	3.3 Coping with Extreme Environmental Temperatures Thermotolerance	87
	3.4 Different Strategies for Improving Thermotolerance	87
	3.5 The Epigenetic Response	89
	3.5.1 Thermal Manipulations During the Postnatal Period	89
	3.5.2 Thermal Manipulations During the Prenatal Period	90
	3.6 Conclusion	95
	References	95
	Part II Mechanistic Basis of Postnatal Co