title: Sedentary behavior during postnatal life is determined by the prenatal environment and exacerbated by postnatal hypercaloric nutrition.
abstract: The discovery of a link between in utero experience and later metabolic and cardiovascular disease is one of the most important advances in epidemiology research of recent years. There is now increasing evidence that alterations in the fetal environment have long-term consequences on metabolic and endocrine pathophysiology in adult life. This process has been termed "fetal programming," and we have shown that undernutrition of the mother during gestation leads to obesity, hypertension, hyperphagia, hyperinsulinemia, and hyperleptinemia in offspring. Using this model of maternal undernutrition throughout pregnancy, we investigated whether prenatal influences may lead to alterations in postnatal locomotor behavior, independent of postnatal nutrition. Virgin Wistar rats were time mated and randomly assigned to receive food either ad libitum (ad libitum group) or at 30% of ad libitum intake (undernourished group). Offspring from UN mothers were significantly smaller at birth than AD offspring. At weaning, offspring were assigned to one of two diets [control or hypercaloric (30% fat)]. At ages of 35 days, 145 days, and 420 days, voluntary locomotor activity was assessed. At all ages studied, offspring from undernourished mothers were significantly less active than offspring born of normal birth weight for all parameters measured, independent of postnatal nutrition. Sedentary behavior in programmed offspring was exacerbated by postnatal hypercaloric nutrition. This work is the first to clearly separate prenatal from postnatal effects and shows that lifestyle choices themselves may have a prenatal origin. We have shown that predispositions to obesity, altered eating behavior, and sedentary activity are linked and occur independently of postnatal hypercaloric nutrition. Moreover, the prenatal influence may be permanent as offspring of undernourished mothers were still significantly less active compared with normal offspring at an advanced adult age, even in the presence of a healthy diet throughout postnatal life.
authors.affiliation: FRS, Liggins Institute, Faculty of Medical and Health Sciences, Univ. of Auckland, Auckland, New Zealand.
authors.forename: M H
authors.initials: MH
authors.lastname: Vickers
authors.forename: B H
authors.initials: BH
authors.lastname: Breier
authors.forename: D
authors.initials: D
authors.lastname: McCarthy
authors.forename: P D
authors.initials: PD
authors.lastname: Gluckman
mesh_terms: D000821:Animal Feed; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D001522:Behavior, Animal / Q000502:physiology*; D005260:Female; D008297:Male; D009043:Motor Activity / Q000502:physiology; D009765:Obesity / Q000503:physiopathology*; D010927:Placental Insufficiency / Q000503:physiopathology*; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar; D012737:Sex Factors