Greenwood / Bell / Vercoe Managing the Prenatal Environment to Enhance Livestock Productivity

1. Auflage 2010
ISBN: 978-90-481-3135-8
Verlag: Springer Netherland
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 298 Seiten, eBook

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.

Zielgruppe

Research

Autoren/Hrsg.

Greenwood, Paul L.

Bell, Alan W.

Vercoe, Philip E.

Viljoen, Gerrit J.

Inhaltsverzeichnis

Quantifying the Magnitude of Prenatal Effects on Productivity.- Postnatal Consequences of the Maternal Environment and of Growth During Prenatal Life for Productivity of Ruminants.- Quantification of Prenatal Effects on Productivity in Pigs.- Managing Prenatal Development of Broiler Chickens to Improve Productivity and Thermotolerance.- Mechanistic Basis of Postnatal Consequences of Fetal Development.- Biological Mechanisms of Fetal Development Relating to Postnatal Growth, Efficiency and Carcass Characteristics in Ruminants.- Mechanistic Aspects of Fetal Development Relating to Postnatal Fibre Production and Follicle Development in Ruminants.- Mechanistic Aspects of Fetal Development Relating to Postnatal Health and Metabolism in Pigs.- Regulatory Aspects of Fetal Growth and Muscle Development Relating to Postnatal Growth and Carcass Quality in Pigs.- Regulators of Fetal and Neonatal Nutrient Supply.- Placental Vascularity: A Story of Survival.- Management and Environmental Influences on Mammary Gland Development and Milk Production.

Leseproben

"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 Factor ß, 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]."