Perinatal Undernutrition and Brain-Derived Neurotrophic Factor
There is now compelling evidence, coming both from animal and human studies, that perinatal alterations such as maternal undernutrition may result in developmental adaptations that permanently change the morphology, physiology, and metabolism in offspring, thereby predisposing individuals to several chronic diseases in adult life. This has led to the notion that some cognitive (depression), psychiatric (schizophrenia), neurodegenerative (Alzheimer disease), and metabolic (hypertension, type 2 diabetes, and obesity) illnesses could be “programmed” during early development. Among the molecules putatively involved in the so-called “Developmental Origin of Health and Adult Diseases,” brain-derived neurotrophic factor is a likely candidate since it plays crucial roles during central nervous system maturation and development. Interestingly, a data have increasingly shown that brain-derived neurotrophic factor exerts an important role in the regulation of energy homeostasis. Indeed, brain-derived neurotrophic factor system alterations are associated with metabolic dysfunctions such as obesity and hyperphagia. We have shown recently that maternal perinatal undernutrition modified both brain-derived neurotrophic factor content and cell proliferation in the central nervous system of the male rat neonate. In view of these data, this chapter selectively focuses on the most recent findings supporting the idea that the brain-derived neurotrophic factor shares the dual role of regulating both energy homeostasis and neural plasticity. It could thus be implicated in the altered perinatal growth and in the increased prevalence of adult diseases frequently observed in offspring of undernourished mothers.
KeywordsAnorexia Nervosa Bulimia Nervosa BDNF Level Adult Disease Central Nervous System Development
Brain-Derived Neurotrophic Factor
Central Nervous System
Developmental Origin of Health and Adult Diseases
50% Food Restriction
Maternal Perinatal Undernutrition
Peripheral Nervous System
p75 Neurotrophin Receptor
Tyrosine Kinase Receptor B
We are grateful to V. Montel, A. Dickes-Coopman and F. Lefevre for technical assistance. This study was supported by the Conseil Régional du Nord-Pas-de-Calais.