Related Articles Elevated plasma norepinephrine inhibits insulin secretion, but adrenergic blockade reveals enhanced ?-cell responsiveness in an ovine model of placental insufficiency at 0.7 of gestation.
J Dev Orig Health Dis. 2013 Oct 1;4(5)
Authors: Macko AR, Yates DT, Chen X, Green AS, Kelly AC, Brown LD, Limesand SW
Abstract
In pregnancies complicated by placental insufficiency (PI), fetal hypoglycemia and hypoxemia progressively worsen during the third trimester, which increases circulating norepinephrine (NE). Pharmacological adrenergic blockade (ADR-block) at 0.9 gestation revealed that NE inhibits insulin secretion and enhanced ?-cell responsiveness in fetuses with PI-induced intrauterine growth restriction (IUGR). NE concentrations in PI fetuses at 0.7 gestation were 3-fold greater compared to age-matched controls but the levels were similar to near-term controls. Therefore, our objective was to determine whether elevations in plasma NE concentrations inhibit insulin secretion and produce compensatory ?-cell responsiveness in PI fetuses at 0.7 gestation. Fetal insulin was measured under basal, glucose-stimulated (GSIS), and glucose potentiated arginine-stimulated (GPAIS) conditions in the absence and presence of an ADR-block. Placental weights were 38% lower (P
J Dev Orig Health Dis. 2013 Oct 1;4(5)
Authors: Macko AR, Yates DT, Chen X, Green AS, Kelly AC, Brown LD, Limesand SW
Abstract
In pregnancies complicated by placental insufficiency (PI), fetal hypoglycemia and hypoxemia progressively worsen during the third trimester, which increases circulating norepinephrine (NE). Pharmacological adrenergic blockade (ADR-block) at 0.9 gestation revealed that NE inhibits insulin secretion and enhanced ?-cell responsiveness in fetuses with PI-induced intrauterine growth restriction (IUGR). NE concentrations in PI fetuses at 0.7 gestation were 3-fold greater compared to age-matched controls but the levels were similar to near-term controls. Therefore, our objective was to determine whether elevations in plasma NE concentrations inhibit insulin secretion and produce compensatory ?-cell responsiveness in PI fetuses at 0.7 gestation. Fetal insulin was measured under basal, glucose-stimulated (GSIS), and glucose potentiated arginine-stimulated (GPAIS) conditions in the absence and presence of an ADR-block. Placental weights were 38% lower (P
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