Synergy of nature and nurture in the development of childhood obesity.
Epidemiological studies suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in human offspring. Animal models provide a means of assessing the independent consequences of altering the pre- vs postnatal environments on a variety of metabolic, physiological and neuroendocrine functions, which lead to the development of offspring obesity, diabetes, hypertension and hyperlipidemia. During the gestational period, maternal malnutrition, obesity, type 1 and type 2 diabetes, and psychological and pharmacological stressors can all promote offspring obesity. Normal postnatal nutrition can sometimes reduce the adverse effect of some of these prenatal factors, but may also exacerbate the development of obesity and diabetes in offspring of dams that are malnourished during gestation. The genetic background of the individual is also an important determinant of outcome when the perinatal environment is perturbed. Individuals with an obesity-prone genotype are more likely to be adversely affected by factors such as maternal obesity and high-fat diets. Many perinatal manipulations are associated with reorganization of the central neural pathways which regulate food intake, energy expenditure and storage in ways that enhance the development of obesity and diabetes in offspring. Both leptin and insulin have strong neurotrophic properties so that an excess or an absence of either of them during the perinatal period may underlie some of these adverse developmental changes. As perinatal manipulations can permanently and adversely alter the systems that regulate energy homeostasis, it behooves us to gain a better understanding of the factors during this period that promote the development of offspring obesity as a means of stemming the tide of the emerging worldwide obesity epidemic.
Neurology Service, VA Medical Center, 385 Tremont Avenue, East Orange, NJ 07018-1095, USA. levin@umdnj.edu
B E
BE
Levin
D000818:Animals; D001835:Body Weight / Q000502:physiology; D002648:Child; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology*; D015444:Exercise; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007328:Insulin / Q000502:physiology; D007774:Lactation; D020738:Leptin / Q000502:physiology; D039382:Maternal Nutritional Physiological Phenomena / Q000502:physiology*; D051379:Mice; D008815:Mice, Inbred Strains; D009765:Obesity / Q000209:etiology* / Q000235:genetics / Q000517:prevention & control; D011247:Pregnancy; D011248:Pregnancy Complications; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D014886:Weaning
D007328:Insulin; D020738:Leptin