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.

This article has been cited by other articles:

				L. Kappeler, C. De Magalhaes Filho, P. Leneuve, J. Xu, N. Brunel, C. Chatziantoniou, Y. Le Bouc, and M. Holzenberger Early Postnatal Nutrition Determines Somatotropic Function in Mice Endocrinology, January 1, 2009; 150(1): 314 - 323. [Abstract] [Full Text] [PDF]

				A. Sagazio, X. Xiao, Z. Wang, M. Martari, and R. Salvatori A single injection of double-stranded adeno-associated viral vector expressing GH normalizes growth in GH-deficient mice J. Endocrinol., January 1, 2008; 196(1): 79 - 88. [Abstract] [Full Text] [PDF]

				M. Thamotharan, M. Garg, S. Oak, L. M. Rogers, G. Pan, F. Sangiorgi, P. W. N. Lee, and S. U. Devaskar Transgenerational inheritance of the insulin-resistant phenotype in embryo-transferred intrauterine growth-restricted adult female rat offspring Am J Physiol Endocrinol Metab, May 1, 2007; 292(5): E1270 - E1279. [Abstract] [Full Text] [PDF]

				M. H. Vickers, P. L. Hofman, P. D. Gluckman, P. E. Lobie, and W. S. Cutfield Combination therapy with acipimox enhances the effect of growth hormone treatment on linear body growth in the normal and small-for-gestational-age rat Am J Physiol Endocrinol Metab, December 1, 2006; 291(6): E1212 - E1219. [Abstract] [Full Text] [PDF]

				S. O Krechowec, M. Vickers, A. Gertler, and B. H Breier Prenatal influences on leptin sensitivity and susceptibility to diet-induced obesity. J. Endocrinol., May 1, 2006; 189(2): 355 - 363. [Abstract] [Full Text] [PDF]

				C. S. Wyrwoll, P. J. Mark, T. A. Mori, I. B. Puddey, and B. J. Waddell Prevention of Programmed Hyperleptinemia and Hypertension by Postnatal Dietary {omega}-3 Fatty Acids Endocrinology, January 1, 2006; 147(1): 599 - 606. [Abstract] [Full Text] [PDF]

				M. Thamotharan, B.-C. Shin, D. T. Suddirikku, S. Thamotharan, M. Garg, and S. U. Devaskar GLUT4 expression and subcellular localization in the intrauterine growth-restricted adult rat female offspring Am J Physiol Endocrinol Metab, May 1, 2005; 288(5): E935 - E947. [Abstract] [Full Text] [PDF]

				I. C. Mcmillen and J. S. Robinson Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming Physiol Rev, April 1, 2005; 85(2): 571 - 633. [Abstract] [Full Text] [PDF]

				M. H. Vickers, B. H. Breier, D. McCarthy, and P. D. Gluckman Sedentary behavior during postnatal life is determined by the prenatal environment and exacerbated by postnatal hypercaloric nutrition Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2003; 285(1): R271 - R273. [Abstract] [Full Text] [PDF]