title: Adult growth hormone treatment reduces hypertension and obesity induced by an adverse prenatal environment.
abstract: The discovery of a link between an adverse in utero environment and the propensity to develop metabolic and cardiovascular disease in adult life is one of the most important advances in epidemiological research of recent Years. Increasing experimental evidence suggests that alterations in the fetal environment may have long-term consequences for the development of metabolic disorders in adult life. This process has been termed 'fetal programming' and we have shown that undernutrition of the mother during gestation leads to development of the metabolic syndrome X during adult life. Striking metabolic similarities exist between syndrome X and untreated GH deficiency (GHD). In the present study we have investigated the effects of GH treatment on blood pressure and metabolic parameters. Virgin Wistar rats (age 75+/-5 days, n=20 per group) were time-mated and randomly assigned to receive food either ad libitum (AD) or 30% of AD intake (UN) throughout pregnancy. At weaning, male offspring were assigned to one of two diets (control or hypercaloric (30% fat)). Systolic blood pressure was measured at day 100 and following twice daily treatment with recombinant bovine GH for 21 days. GH treatment increased body weights in all treated animals but significantly reduced retroperitoneal and gonadal fat pad weights. Following GH treatment, systolic blood pressure was markedly decreased in all UN offspring. Saline-treated animals showed no change in systolic blood pressure over the treatment period. GH treatment increased heart-to-body weight ratio in all GH-treated animals. Our data demonstrated that GH treatment reduces hypertension and improves cardiovascular function in animals exposed to adverse environmental conditions during fetal or postnatal life.
authors.affiliation: The Liggins Institute for Medical Research, Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand. m.vickers@auckland.ac.nz
authors.forename: M H
authors.initials: MH
authors.lastname: Vickers
authors.forename: B A
authors.initials: BA
authors.lastname: Ikenasio
authors.forename: B H
authors.initials: BH
authors.lastname: Breier
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D002149:Energy Intake; D005260:Female; D005317:Fetal Growth Retardation; D013006:Growth Hormone / Q000627:therapeutic use*; D006973:Hypertension / Q000188:drug therapy* / Q000196:embryology* / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D009765:Obesity / Q000188:drug therapy* / Q000196:embryology* / Q000378:metabolism; D009929:Organ Size; D011247:Pregnancy; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
chemical_list: D001786:Blood Glucose; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone