REVIEW PAPER
Prenatal glucocorticoids can programme postnatal development
1
Department of Animal Biochemistry and Physiology, Faculty of Veterinary Medicine, University of Life Sciences, Lublin, Poland
2
Department of Comparative Anatomy and Anthropology, Maria Curie-Skłodowska University, Lublin, Poland
Corresponding author
Ewa Tomaszewska
Faculty of Veterinary Medicine, Department of Animal Biochemistry and Physiology, University of Life Sciences, Akademicka 13, 20-950 Lublin, Poland, tel.: 81 445 69 63.
Faculty of Veterinary Medicine, Department of Animal Biochemistry and Physiology, University of Life Sciences, Akademicka 13, 20-950 Lublin, Poland, tel.: 81 445 69 63.
J Pre Clin Clin Res. 2011;5(1):7–11
KEYWORDS
ABSTRACT
Endogenous steroid hormones play a fundamental role in the prenatal development of important vital systems, but when their concentration is long-time enhanced they have a negative impact on the postnatal physiological processes. Prenatal programming is widely used in the context of the permanent alteration of foetal physiological processes. These are caused by factors acting during a critical period of development called the window of the development. Different factors may programme foetal maturity and enhance survival ability after the birth, and may result in disadvantageous consequences in postnatal life. Many studies have shown a relationship between alterations induced by the impact of the mother during pregnancy on the embryo or foetal development, and many consequences which are observed in their off spring. Synthetic glucocorticoids (GCs) given to pregnant females (experimentally or therapeutically), and the increase of endogenous GCs caused by different stressors, lead to identical changes in the process of foetus development. This review focuses on the impact of the prenatal overload with synthetic glucocorticoids on the postnatal development of both humans and experimental animals. It is not known whether these alterations are transient or permanent after the birth, or if they persist, and the extent to which they may be reversed therapeutically.
REFERENCES (37)
1.
Gill JW, Hosking BJ, Egan AR. Prenatal programing of mammalian growth – a review of the role of steroids. Liv Prod Sci 1998;54:251- 267.
2.
Han VKM, Carter AM. Control of growth and development of the feto-placental unit. Curr Opin Pharmacol 2001;1:632-640.
3.
O`Regan D, Welberg LL, Holmes MC, Seckl JR.: Glucocorticoid programming of pituitary-adrenal function: mechanisms and physiological consequences. Semin Neonatol 2001;6:319-329.
4.
Smith NH, Ozanne SE. Intrauterine origins of metabolic disease. Rev Gynaecol Perinat Pract 2006;6:211-217.
5.
Holemans K, Aertis L, Van Assche A. Fetal growth and long-term consequences in animal models of growth retardation. Eur J Obstet Gynecol 1998;81:149-156.
6.
Simmons RA, Templeton LJ, Gertz SJ. Intrauterine growth retardation leads to the development of type 2 diabetes in the rat. Diabetes 2001;50:2279-2286.
7.
Newnham JP, Moss TJ. Antenatal glucocorticoids and growth: single versus multiple doses in animal and human studies. Semin Neonatol 2001;6:285-292.
8.
Klemcke HG, McGuire WJ, Christenson RK. Cortisol concentration in early porcine embryos. Life Sci 1999;64:1307-1312.
9.
Van Prag HM, De Kloet R, Van Os J. Stress, the brain and depression. Cambridge University Press, Cambridge (UK) 2004.
10.
Seckl JR. Glucocorticoid programming of the fetus; adult phenotypes and molecular mechanisms. Mol Cell Endocrinol 2001;185:61-71.
11.
Kawata M, Yuri K, Ozawa H, Nishi M, Ito T, Hu Z, Lu H, Yoshida M. Steroid hormones and their receptors in the brain. J Steroid Biochem Mol Biol 1998;65:273-280.
12.
Matthews SG. Antenatal glucocorticoids and the development brain: mechanisms of action. Semin Neonatol 2001;6:309-317.
13.
Śliwa E, Dobrowolski P. Perinatal programing of skeletal system. J Pre- Clin Clin Res 2007;1:111-117.
14.
Williams MT, Davis HN, McCrea AE, Hennessy MB. Stress during pregnancy alters the off spring hypothalamic, pituitary, adrenal, and testicular response to isolation on the day of weaning. Neurotoxicol Teratol 1999;21:653-659.
15.
Clift on VL, Murphy VE. Maternal asthma as a model for examining fetal sex-specifi c eff ects on maternal physiology and placental mechanisms that regulate human fetal growth. Placenta 2004;25:S45-S52.
16.
Engle MJ, Kemnitz JW, Rao TJ, Perelman RH, Farrell PM: Eff ects of maternal dexamethasone therapy on fetal lung development in the rhesus monkey. Amer J Perinatol 1996;13:399-407.
17.
Maccari S, Darnaudery M, Morley-Fletcher S, Zuena AR, Cinque C, Van Reeth O. Prenatal stress and long-term consequences: implications of glucocorticoids hormones. Neurosci Biobehav Rev 2003;27:119-127.
18.
Slotkin TA, Barnes GA, McCook EC, Seidker FJ. Programming of brainstem serotonin transporter development by prenatal glucocorticoids. Develop Brain Res 1996;93:155-161.
19.
Nagano M, Ozawa H, Suzuki H. Prenatal dexamethasone exposure aff ects anxiety like behaviour and neuroendocrine systems in an agedependent manner. Neurosci Res 2008;60:364-371.
20.
Redrobe JP, Dumont Y, Fournier A, Quirion R. Th e neuropeptide Y (NPY) Y1 receptor subtype mediates NPY-induced antidepressant-like activity in the mouse forced swimming test. Neuropsychopharmacol 2002;26:615-624.
21.
Xu R-J, Mellor DJ, Birtles MJ, Reynolds GW, Simpson H. Impact of intrauterine growth retardation on the gastrointestinal tract and the pancreas in newborn pigs. J Pediatr Gastroenterol Nutr 1994;18:231- 240.
22.
Jahnukainen T, Chen M, Berg U, Celsi G. Antenatal glucocorticoids and renal function aft er birth. Semin Neonatol 2001;6:351-355.
23.
Jiang B, Godfrey KM, Martyn CN. Birth weight and cardiac structure in children. Pediatrics 2006;117:257-261.
24.
McMillen IC, Adams MB, Ross JT. Fetal growth restriction: adaptations and consequences. Reproduction 2001;122:195-204.
25.
Petry CJ, Ozanne SE, Hales CN. Programming of intermediary metabolism. Mol Cell Endocrinol 2001;185:81-91.
26.
Sangild PT, Fowden AL, Trahair JF. How does the foetal gastrointestinal tract develop in preparation for enteral nutrition aft er birth? Liv Produc Sci 2000;66:141-150.
27.
Śliwa E, Dobrowolski P, Tatara MR, Piersiak T, Siwicki A, Rokita E. Alpha-ketoglutarate protects the liver of piglets exposed during prenatal life to chronic excess of dexamethasone from metabolic and structural changes. J Anim Physiol Anim Nutr 2009;93:192-202.
28.
Tomaszewska E, Dobrowolski P, Puzio I. Postnatal administration of 2-oxoglutaric acid improves the intestinal barrier aff ected by the prenatal action of dexamethasone in pigs. Nutrition 2011, doi:10.1016/ j.nut.2011.05.010.
29.
Breier BH, Vickers MH, Ikenasio BA, Chan KY, Wong WP. Fetal programming of appetite and obesity. Mol Cell Endocrinol 2001;185:73- 79.
30.
Śliwa E, Dobrowolski P, Piersiak T. Bone development of suckling piglets aft er prenatal, neonatal or perinatal treatment with dexamethasone. J Anim Physiol Anim Nutr 2010;94:293-306.
31.
Jobe A, Wada N, Berry LM, Ikegami M, Ervin MG. Single and repetitive maternal glucocorticoids exposures reduce fetal growth in sheep. Amer J Obstet Gynecol 1998;178:880-885.
32.
Śliwa E, Tatara MR, Nowakowski H, Pierzynowski SG, Studziński T. Eff ect of maternal dexamethasone and alpha-ketoglutarate administration on skeletal development during the last three weeks of prenatal life in pigs. J Matern Fetal Neonatal Med 2006;19:489-493.
33.
Śliwa E, Dobrowolski P, Puzio I. Prenatal programming of articular cartilage in pigs. Bone 2010;47:S78.
34.
Hofb auer LC, Kuhne CA, Viereck V. Th e OPG/RANKL/RANK system in metabolic bone diseases. J Musculoskel Neuronal Interact 2004;4:268-275.
35.
Challis JRG, Sloboda D, Matthews SG, Holloway A, Alfaidy N, Patel FA, Whittle W, Fraser M, Moss TJ, Newnham J. Th e fetal placental hypothalamic-pituitary-adrenal (HPA) axis, parturition and post natal health. Mol Cell Endocrinol 2001;185:135-144.
36.
Minisola S, Fitzpatrick L. Bone physiology. In: EA Eugster, OH Pescovitz (ed) Developmental endocrinology. From research to clinical practice. Humana Press, New Jersey 2002:193-217.
37.
Rijnberk A. Clinical endocrinology of dogs and cats. Kluwer Academic Publishers, Dordrecht, Th e Netherlands 1996.
We process personal data collected when visiting the website. The function of obtaining information about users and their behavior is carried out by voluntarily entered information in forms and saving cookies in end devices. Data, including cookies, are used to provide services, improve the user experience and to analyze the traffic in accordance with the Privacy policy. Data are also collected and processed by Google Analytics tool (more).
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.