Effects of Pituitary Hormone Deficiency on Growth and Glucose Metabolism of the Sheep Fetus

Fowden, Abigail L.; Forhead, Alison J.

doi:10.1210/en.2007-0639

Cited by 6 publications

(9 citation statements)

References 41 publications

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“…The sheep is one of the most commonly and extensively investigated precocial species in biomedical studies on human pregnancy (17,19,25,32). These data demonstrate a markedly (ϳ 30%) increased fetal weight in OB vs. C ewes at midgestation, indicating a greater fetal growth trajectory in OB females during the first half of gestation.…”

Section: Discussionmentioning

confidence: 78%

Maternal obesity and overnutrition alter fetal growth rate and cotyledonary vascularity and angiogenic factor expression in the ewe

Zhu

Zhang

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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In pregnant sheep, maternal:fetal exchange occurs across placentomes composed of placental cotyledonary and uterine caruncular tissues. Recently, we reported that fetal weights of obese (OB) ewes [fed a diet of 150% of National Research Council (NRC) recommendations] were approximately 30% greater than those of control (C) ewes (fed a diet 100% of NRC recommendations) at midgestation (MG), but fetal weights were similar in late gestation (LG). Transplacental nutrient exchange is dependent on placental blood flow, which itself is dependent on placental vascularity. The current study investigated whether the observed initial faster and subsequent slower fetal growth rate of OB compared with C was associated with changes in cotyledonary vascularity and expression of angiogenic factors (vascular endothelial growth factor, fibroblast growth factor-2, placental growth factor, angiopoietin-1 and -2). Cotyledonary arteriole diameters were markedly greater (P < 0.05) in OB than C ewes at MG, but while arteriole diameter of C ewes increased (P < 0.05) from MG to LG, they remained unchanged in OB ewes. Cotyledonary arterial angiogenic factors mRNA and protein expression were lower (P < 0.05) in OB than C ewes at MG and remained low from MG to LG. In contrast, mRNA levels of angiogenic factors in C ewes declined from high levels at MG to reach those of OB ewes by LG. The increase in cotyledonary arteriole diameter in early to MG may function to accelerate fetal growth rate in OB ewes, while the decreased cotyledonary arterial angiogenic factors from MG-LG may function to protect the fetus from excessive placental vascular development, increased maternal nutrient delivery, and excessive weight gain.

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Section: Discussionmentioning

confidence: 78%

Maternal obesity and overnutrition alter fetal growth rate and cotyledonary vascularity and angiogenic factor expression in the ewe

Zhu

Zhang

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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“…1). In part, the effects of fetal hypophysectomy are the result of multiple endocrine deficiencies as there are changes in the fetal concentrations of IGFs, GH, thyroid hormones and cortisol in hypophysectomised fetuses during late gestation [9]. Generally, the growth stimulatory hormones act as signals of nutrient plenty and rise in concentration in the fetus with increases in the availability of glucose, amino acids and oxygen [5].…”

Section: Growth Stimulatory Hormonesmentioning

confidence: 99%

Endocrine Regulation of Feto-Placental Growth

Fowden

Forhead²

2009

Horm Res Paediatr

117

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Hormones are both growth stimulatory and growth inhibitory in utero. They regulate tissue growth and development by controlling the rates of cell proliferation, apoptosis and differentiation in many fetal tissues. They also signal the level of resources available for intrauterine growth to the fe- tal tissues and relay back to the placenta the degree of mismatch between the actual fetal nutrient supply and the fetal nutrient demands for growth. They affect intrauterine growth by anabolic and catabolic actions on fetal metabolism and by altering the nutrient transfer capacity and endocrine function of the placenta. By modifying the fetal growth trajectory, hormones have a central role in programming development in utero and in determining the phenotypic outcome of changes in feto-placental growth during adverse intrauterine conditions. This review examines the role of hormones in feto-placental growth with particular emphasis on insulin, the insulin-like growth factors and glucocorticoids.

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“…Fetal plasma epinephrine and norepinephrine concentrations were measured by HPLC using electrochemical detection, as previously described in detail (18). The samples were prepared by absorption of 250 l of plasma onto acid-washed alumina, and 20-l aliquots of the 100-l perchloric acid elutes were injected onto the column.…”

Section: Hormone Analysesmentioning

confidence: 99%

Effects of acute acidemia on the fetal cardiovascular defense to acute hypoxemia

Thakor¹,

Giussani²

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Thakor AS, Giussani DA. Effects of acute acidemia on the fetal cardiovascular defense to acute hypoxemia. Am J Physiol Regul Integr Comp Physiol 295: R90 -R99, 2009. First published October 15, 2008 doi:10.1152/ajpregu.90689.2008.-In complicated pregnancy, fetal hypoxemia rarely occurs in isolation but is often accompanied by fetal acidemia. There is growing clinical concern about the combined effects of fetal hypoxemia and fetal acidemia on neonatal outcome. However, the effects on the fetal defense responses to acute hypoxemia during fetal acidemia are not well understood. This study tested the hypothesis that fetal acidemia affects the fetal defense responses to acute hypoxemia. The hypothesis was tested by investigating, in the late-gestation sheep fetus surgically prepared for long-term recording, the in vivo effects of acute fetal acidemia on 1) the fetal cardiovascular responses to acute hypoxemia and 2) the neural and endocrine mechanisms mediating these responses. Under general anesthesia, five sheep fetuses at 0.8 gestation were instrumented with catheters and Transonic flow probes around the femoral and umbilical arteries. After 5 days, animals were subjected to an acute hypoxemia protocol during intravenous infusion of saline or treatment with acidified saline. Treatment with acidified saline reduced fetal basal pH from 7.35 Ϯ 0.01 to 7.29 Ϯ 0.01 but did not alter basal cardiovascular variables, blood glucose, or plasma concentrations of catecholamines, ACTH, and cortisol. During hypoxemia, treatment with acidified saline increased the magnitude of the fetal bradycardia and femoral vasoconstriction and concomitantly increased chemoreflex function and enhanced the increments in plasma concentrations of catecholamines, ACTH, and cortisol. Acidemia also reversed the increase in umbilical vascular conductance during hypoxemia to vasoconstriction. In conclusion, the data support our hypothesis and show that acute acidemia markedly alters fetal hemodynamic, metabolic, and endocrine responses to acute hypoxemia.

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Effects of Pituitary Hormone Deficiency on Growth and Glucose Metabolism of the Sheep Fetus

Cited by 6 publications

References 41 publications

Maternal obesity and overnutrition alter fetal growth rate and cotyledonary vascularity and angiogenic factor expression in the ewe

Maternal obesity and overnutrition alter fetal growth rate and cotyledonary vascularity and angiogenic factor expression in the ewe

Endocrine Regulation of Feto-Placental Growth

Effects of acute acidemia on the fetal cardiovascular defense to acute hypoxemia

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