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首页> 外文期刊>American Journal of Physiology >Chronic exposure to elevated norepinephrine suppresses insulin secretion in fetal sheep with placental insufficiency and intrauterine growth restriction.
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Chronic exposure to elevated norepinephrine suppresses insulin secretion in fetal sheep with placental insufficiency and intrauterine growth restriction.

机译：长期暴露于升高的去甲肾上腺素会抑制胎盘功能不全和子宫内生长受限的胎羊的胰岛素分泌。

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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 (alpha) and propranolol (beta). IUGR fetuses were hypoglycemic and hypoxemic and had lower GSIS responsiveness (P < or = 0.05) than control fetuses. IUGR fetuses also had elevated plasma norepinephrine (3,264 +/- 614 vs. 570 +/- 86 pg/ml; P < or = 0.05) and epinephrine (164 +/- 32 vs. 60 +/- 12 pg/ml; P < or = 0.05) concentrations. In control fetuses, adrenergic inhibition increased baseline plasma insulin concentrations (1.7-fold, P < or = 0.05), whereas during hyperglycemia insulin was not different. A greater (P < or = 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 < or = 0.05) with adrenergic antagonists. GSIS responsiveness, measured by the change in insulin, was higher (8.9-fold, P < or = 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 beta-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 alpha(1D), alpha(2A), and alpha(2B) in a cohort of fetuses that were naive to the antagonists. Therefore, norepinephrine suppression of insulin secretion was maintained, in part, by upregulating adrenergic receptor expression, but the beta-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.
机译：在这项研究中，我们检查了具有胎盘功能不全引起的宫内生长受限（IUGR）的绵羊胎儿的慢性去甲肾上腺素对胰岛素分泌的抑制作用。在存在或不存在肾上腺素能受体拮抗剂酚妥拉明（α）和心得安（β）的情况下，用方波高血糖钳夹法测量葡萄糖刺激的胰岛素分泌（GSIS）。 IUGR胎儿是低血糖和低氧血症，并且与对照胎儿相比，其GSIS反应性较低（P <或= 0.05）。 IUGR胎儿的血浆去甲肾上腺素（3,264 +/- 614 vs.570 +/- 86 pg / ml; P <或= 0.05）和肾上腺素（164 +/- 32 vs. 60 +/- 12 pg / ml; P <或= 0.05）浓度。在对照胎儿中，肾上腺素抑制增加了基线血浆胰岛素浓度（1.7倍，P <或= 0.05），而在高血糖期间胰岛素没有差异。在IUGR胎儿中发现对肾上腺素抑制的反应更大（P <或= 0.05），基线时平均血浆胰岛素浓度增加了4.9倍，高血糖时增加了7.1倍。与对照组不同，肾上腺素能拮抗剂使基础血浆葡萄糖浓度下降（P <或= 0.05）。肾上腺素能抑制的IUGR胎儿的GSIS反应性（通过胰岛素的变化来衡量）高于对照组（8.9倍，P <或= 0.05），高于对照组（1.8倍，不显着），表明去甲肾上腺素抑制了IUGR胎儿的胰岛素分泌。令人惊讶的是，在IUGR胎儿中，肾上腺素能抑制导致更大的GSIS反应性，因为β细胞质量降低了56％，最大刺激性胰岛素反应趋于（P <0.1）高于对照组。这种持续的去甲肾上腺素抑制作用似乎可以部分归因于天真的拮抗剂中一群肾上腺素能受体α（1D），α（2A）和α（2B）的mRNA浓度较高。因此，通过上调肾上腺素能受体的表达来维持去甲肾上腺素对胰岛素分泌的抑制，但是β细胞似乎也可以补偿增强的GSIS。这些发现可能开始解释为什么如果出生后突然去甲去甲肾上腺素下降，IUGR婴儿就有增加葡萄糖需求的倾向。

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