scholarly journals Intrauterine growth restriction transiently delays alveolar formation and disrupts retinoic acid receptor expression in the lung of female rat pups

2013 ◽  
Vol 73 (5) ◽  
pp. 612-620 ◽  
Author(s):  
Lisa Joss-Moore ◽  
Travis Carroll ◽  
Yan Yang ◽  
Melanie Fitzhugh ◽  
Drew Metcalfe ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Intrauterine Growth Restriction ◽  
Retinoic Acid Receptor ◽  
Growth Restriction ◽  
Receptor Expression ◽  
Female Rat ◽  
Acid Receptor ◽  
Intrauterine Growth ◽  
Rat Pups ◽  
Alveolar Formation

scholarly journals Chronic exposure to elevated norepinephrine suppresses insulin secretion in fetal sheep with placental insufficiency and intrauterine growth restriction

2010 ◽  
Vol 298 (4) ◽  
pp. E770-E778 ◽  
Author(s):  
Rafael A. Leos ◽  
Miranda J. Anderson ◽  
Xiaochuan Chen ◽  
Juliana Pugmire ◽  
K. Arbor Anderson ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Intrauterine Growth Restriction ◽  
Adrenergic Receptor ◽  
Plasma Insulin ◽  
Placental Insufficiency ◽  
Growth Restriction ◽  
Receptor Expression ◽  
Plasma Norepinephrine ◽  
Fetal Sheep ◽  
Intrauterine Growth

In this study, we examined chronic norepinephrine suppression of insulin secretion in sheep fetuses with placental insufficiency-induced intrauterine growth restriction (IUGR). Glucose-stimulated insulin secretion (GSIS) was measured with a square-wave hyperglycemic clamp in the presence or absence of adrenergic receptor antagonists phentolamine (α) and propranolol (β). IUGR fetuses were hypoglycemic and hypoxemic and had lower GSIS responsiveness ( P ≤ 0.05) than control fetuses. IUGR fetuses also had elevated plasma norepinephrine (3,264 ± 614 vs. 570 ± 86 pg/ml; P ≤ 0.05) and epinephrine (164 ± 32 vs. 60 ± 12 pg/ml; P ≤ 0.05) concentrations. In control fetuses, adrenergic inhibition increased baseline plasma insulin concentrations (1.7-fold, P ≤ 0.05), whereas during hyperglycemia insulin was not different. A greater ( P ≤ 0.05) response to adrenergic inhibition was found in IUGR fetuses, and the average plasma insulin concentrations increased 4.9-fold at baseline and 7.1-fold with hyperglycemia. Unlike controls, basal plasma glucose concentrations fell ( P ≤ 0.05) with adrenergic antagonists. GSIS responsiveness, measured by the change in insulin, was higher (8.9-fold, P ≤ 0.05) in IUGR fetuses with adrenergic inhibition than controls (1.8-fold, not significant), showing that norepinephrine suppresses insulin secretion in IUGR fetuses. Strikingly, in IUGR fetuses, adrenergic inhibition resulted in a greater GSIS responsiveness, because β-cell mass was 56% lower and the maximal stimulatory insulin response tended ( P < 0.1) to be higher than controls. This persistent norepinephrine suppression appears to be partially explained by higher mRNA concentrations of adrenergic receptors α1D, α2A, and α2B in a cohort of fetuses that were naïve to the antagonists. Therefore, norepinephrine suppression of insulin secretion was maintained, in part, by upregulating adrenergic receptor expression, but the β-cells also appeared to compensate with enhanced GSIS. These findings may begin to explain why IUGR infants have a propensity for increased glucose requirements if norepinephrine is suddenly decreased after birth.

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