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Increasing evidence from human epidemiological studies suggests that poor growth before birth is associated with postnatal growth retardation and the development of cardiovascular disease in adulthood. We have shown previously that nutritional deprivation in the pregnant rat leads to intrauterine growth retardation (IUGR), postnatal growth failure, changes in the endocrine parameters of the somatotrophic axis, and to increased blood pressure in later life. In the present study, we investigated whether administration of insulin-like growth factor-I (IGF-I) or bovine growth hormone (GH) during pregnancy could prevent IUGR and/or alter long-term outcome. Dams from day 1 of pregnancy throughout gestation received a diet of ad libitum available food or a restricted dietary intake of 30% of ad libitum fed dams. From day 10 of gestation, dams were treated for 10 days with three times daily subcutaneous injections of saline (100 microl), IGF-I (2 micrograms/g body weight) or GH (2 micrograms/g body weight). Maternal weight gain was significantly increased (P<0.001) in ad libitum fed dams treated with GH, (98.9+/-4.73 g) compared with the IGF-I (80.5+/-2.17 g) and saline-treated (70.7+/-2.65 g) groups. There was a small increase in maternal weight gain (P<0.06) in 30% ad libitum fed dams following GH (16.3+/-2.47 g) and IGF-I (15.8+/-1.97 g) treatment compared with saline (9.2+/-1.96 g). Whole spleen, kidney and carcass weights were significantly (P<0.05) increased in ad libitum fed and 30% ad libitum fed dams with GH treatment. Circulating IGF-I was significantly increased (P<0.001) in ad libitum fed dams with both IGF-I (369.6+/-32.33 ng/ml) and GH (457.9+/-33.32 ng/ml) compared with saline treatment (211.7+/-14.02 ng/ml), and with GH (223.4+/-23.72 ng/ml) compared with saline treatment (112.0+/-7.33 ng/ml) in 30% ad libitum fed dams. Circulating GH binding protein (GHBP) levels were significantly reduced (P<0.05) in GH-treated (299.1+/-51.54 ng/ml) compared with saline-treated (503.9+/-62.43 ng/ml) ad libitum fed dams, but were not altered in 30% ad libitum fed dams. There was no significant effect of either IGF-I or GH treatment on fetal weight, placental weight, fetal organ weights or circulating IGF-I levels in both ad libitum fed and 30% ad libitum fed fetuses. Offspring of 30% ad libitum fed dams remained significantly growth retarded postnatally and showed elevated blood pressure in later life. The increased maternal weight gain following IGF-I or GH administration, without an effect on fetal and placental weights, suggests a modification in the mode of maternal nutrient repartitioning during mid to late pregnancy at the expense of the fetus.
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Pregnant ewes were exposed chronically to thermoneutral (TN; 20+/-2 degrees C, 30% relative humidity; n=8) or hyperthermic (HT; 40+/-2 degrees C 12 h/day, 35+/-2 degrees C 12 h/day, 30% relative humidity, n=6) environments between days 37 and 93 of pregnancy. Ewes were killed following 56 days of exposure to either environment (days in treatment (dit)), corresponding to 93+/-1 day post coitus (dpc). Maternal core body temperatures (CBT) in HT ewes were significantly elevated above the TN ewes (HT; 39.86+/-0.1 degrees C vs TN; 39.20+/-0.1 degrees C; P<0.001). Both groups of animals displayed circadian CBT, though HT ewes had elevated amplitudes (HT; 0.181+/-0.002 degrees C vs TN; 0.091+/-0.002 degrees C; P<0.001) and increased phase shift constants (HT; 2100 h vs TN; 1800 h; P<0.001). Ewes exposed to chronic heat stress had significantly reduced progesterone and ovine placental lactogen (oPL) concentrations from 72 and 62 dpc respectively (P<0.05), corresponding to approximately 30 dit. However, when compared with the TN ewes, HT cotyledonary tissue oPL mRNA and protein concentrations were not significantly different (P>0.1). Prolactin concentrations rose immediately upon entry into the HT environment, reaching concentrations approximately four times that of TN ewes, a level maintained throughout the study (HT; 216.31+/-32.82 vs TN; 54. 40+/-10.0; P<0.0001). Despite similar feed intakes and euglycemia in both groups of ewes, HT fetal body weights were significantly reduced when compared with TN fetuses (HT; 514.6+/-48.7 vs TN; 703. 4+/-44.8; P<0.05), while placental weights (HT; 363.6+/-63.3 vs TN; 571.2+/-95.9) were not significantly affected by 56 days of heat exposure. Furthermore, the relationship between body weight and fetal length, the ponderal index, was significantly reduced in HT fetuses (HT; 3.01+/-0.13 vs TN; 3.57+/-0.18; P<0.05). HT fetal liver weights were also significantly reduced (HT; 27.31+/-4.73 vs TN; 45.16+/-6.16; P<0.05) and as a result, the brain/liver weight ratio was increased. This study demonstrates that chronic heat exposure lowers circulating placental hormone concentrations. The observation that PL mRNA and protein contents are similar across the two treatments, suggests that reduced hormone concentrations are the result of impaired trophoblast cell development, specifically trophoblast migration. Furthermore, the impact of heat exposure during maximal placental growth is great enough to restrict early fetal development, even before the fetal maximal growth phase (100 dpc-term). These data highlight that intrauterine growth retardation (IUGR) may result primarily from placental trophoblast cell dysfunction, and secondarily from later reduced placental size.
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a smaller-than-normal placenta, with or without specific transporter deficiencies, that restricts nutrient flow from the mother to the fetus and uniquely causes intrauterine growth restriction (IUGR; Molteni et al . 1978 , Marconi et al . 2006
Basic Medical College of Nanyang Medical University, Nanyang, China
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Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan, China
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pregnancy in the United States ( Signorello & McLaughlin 2004 ). Previous studies have indicated that prenatal caffeine exposure (PCE) resulted in adverse birth outcomes, including intrauterine growth retardation (IUGR) ( Fortier et al. 1993 , Chen et al
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Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan, China
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Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan, China
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retardation (IUGR) ( Spohr et al. 1993 , Nykjaer et al. 2014 ), with long-term impact on the offspring’s reproductive function ( Wilson & Handa 1997 , Dupont et al. 2012 ). A previous study showed that PEE can disrupt the development and function of
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al . 2007 ). In humans, reduced growth before birth is also associated with altered left ventricular mass ( Vijayakumar et al . 1995 ), with intrauterine growth-restricted (IUGR) fetuses having a larger heart relative to their body weight ( Veille
Departments of Physiology and Pharmacology, Obstetrics and Gynecology, The Children's Health Research Institute, The Lawson Health Research Institute, The University of Western Ontario, London, Ontario, Canada N6A 5C1
Departments of Physiology and Pharmacology, Obstetrics and Gynecology, The Children's Health Research Institute, The Lawson Health Research Institute, The University of Western Ontario, London, Ontario, Canada N6A 5C1
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Departments of Physiology and Pharmacology, Obstetrics and Gynecology, The Children's Health Research Institute, The Lawson Health Research Institute, The University of Western Ontario, London, Ontario, Canada N6A 5C1
Departments of Physiology and Pharmacology, Obstetrics and Gynecology, The Children's Health Research Institute, The Lawson Health Research Institute, The University of Western Ontario, London, Ontario, Canada N6A 5C1
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Departments of Physiology and Pharmacology, Obstetrics and Gynecology, The Children's Health Research Institute, The Lawson Health Research Institute, The University of Western Ontario, London, Ontario, Canada N6A 5C1
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Departments of Physiology and Pharmacology, Obstetrics and Gynecology, The Children's Health Research Institute, The Lawson Health Research Institute, The University of Western Ontario, London, Ontario, Canada N6A 5C1
Departments of Physiology and Pharmacology, Obstetrics and Gynecology, The Children's Health Research Institute, The Lawson Health Research Institute, The University of Western Ontario, London, Ontario, Canada N6A 5C1
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Departments of Physiology and Pharmacology, Obstetrics and Gynecology, The Children's Health Research Institute, The Lawson Health Research Institute, The University of Western Ontario, London, Ontario, Canada N6A 5C1
Departments of Physiology and Pharmacology, Obstetrics and Gynecology, The Children's Health Research Institute, The Lawson Health Research Institute, The University of Western Ontario, London, Ontario, Canada N6A 5C1
Departments of Physiology and Pharmacology, Obstetrics and Gynecology, The Children's Health Research Institute, The Lawson Health Research Institute, The University of Western Ontario, London, Ontario, Canada N6A 5C1
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Introduction Epidemiological evidence suggests that adverse events in utero (e.g. placental insufficiency-induced intrauterine growth restriction (PI-IUGR)) can permanently alter physiological processes leading to hypertension and type 2 diabetes
School of Animal and Comparative Biomedical Sciences, University of Arizona, Tucson, Arizona, USA
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-induced intrauterine growth restriction (PI-IUGR), glucose-stimulated insulin secretion (GSIS) was attenuated, in part, by elevated catecholamine concentrations ( Limesand et al. 2006 , Macko et al. 2016 ). Pharmacological adrenergic blockade in IUGR sheep fetuses
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Rodent models have played a key role in our understanding of adipokines in the development of a range of programming-mediated disorders ( Bouret 2010 , Vickers & Sloboda 2012 a ). In the setting of intrauterine growth restriction (IUGR), the predictive
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programming of postnatal metabolism has been demonstrated in a number of species using a range of different techniques to induce intrauterine growth restriction (IUGR) including maternal stress and glucocorticoid administration (see McMillen & Robinson 2005
