Table of Contents

The contribution of heredity to clinical obesity.
Monogenic disorders within the energy balance pathway.
Ciliary syndromes and obesity.
Genome-wide association studies and human population obesity.
Obesity: nature or nurture?.
Known clinical epigenetic disorders with an obesity phenotype: Prader-Willi syndrome and the GNAS locus.
Evidence for epigenetic changes as a cause of clinical obesity.
Epigenetic changes associated with intrauterine growth retardation and adipogenesis.
Exposure to diabetes in utero, offspring growth, and risk for obesity.
Maternal weight gain during pregnancy and obesity in the offspring.
Intrauterine growth restriction, small for gestational age, and experimental obesity.
Experimental models for maternal obesity and high-fat diet during pregnancy and programmed obesity in the offspring.
High-carbohydrate intake only during the suckling period results in adult-onset obesity in mother as well as offspring.
Prenatal stress, glucocorticoids, and the metabolic syndrome.
Hypothalamic fetal programming of energy homeostasis.
Adipocyte development and experimental obesity.
The Obesogen hypothesis of obesity: overview and human evidence.
Perinatal exposure to endocrine disrupting chemicals with estrogenic activity and the development of obesity.
The role of environmental obesogens in the obesity epidemic. This volume will explore the epidemiology and the basic mechanisms of each of these prenatal phenomena, in an attempt to explain the role of the prenatal environment in promoting postnatal weight gain. This information will contribute to resolving the nature-nurture controversy. This information provides guidance to clinical practitioners involved in both prenatal and postnatal care. This volume further stimulates research into underlying mechanisms and prevention and treatment of this phenomenon.