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首页> 外文期刊>American Journal of Physiology >Decreased nutrient-stimulated insulin secretion in chronically hypoglycemic late-gestation fetal sheep is due to an intrinsic islet defect.
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Decreased nutrient-stimulated insulin secretion in chronically hypoglycemic late-gestation fetal sheep is due to an intrinsic islet defect.

机译：慢性低血糖晚期妊娠胎羊的营养素刺激的胰岛素分泌减少是由于内在的胰岛缺陷所致。

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摘要

We measured in vivo and in vitro nutrient-stimulated insulin secretion in late gestation fetal sheep to determine whether an intrinsic islet defect is responsible for decreased glucose-stimulated insulin secretion (GSIS) in response to chronic hypoglycemia. Control fetuses responded to both leucine and lysine infusions with increased arterial plasma insulin concentrations (average increase: 0.13 +/- 0.05 ng/ml leucine; 0.99 +/- 0.26 ng/ml lysine). In vivo lysine-stimulated insulin secretion was decreased by chronic (0.37 +/- 0.18 ng/ml) and acute (0.27 +/- 0.19 ng/ml) hypoglycemia. Leucine did not stimulate insulin secretion following acute hypoglycemia but was preserved with chronic hypoglycemia (0.12 +/- 0.09 ng/ml). Isolated pancreatic islets from chronically hypoglycemic fetuses had normal insulin and DNA content but decreased fractional insulin release when stimulated with glucose, leucine, arginine, or lysine. Isolated islets from control fetuses responded to all nutrients. Therefore, chronic late gestation hypoglycemia causes defective in vitro nutrient-regulated insulin secretion that is at least partly responsible for diminished in vivo GSIS. Chronic hypoglycemia is a feature of human intrauterine growth restriction (IUGR) and might lead to an islet defect that is responsible for the decreased insulin secretion patterns seen in human IUGR fetuses and low-birth-weight human infants.
机译：我们测量了妊娠晚期胎羊的体内和体外营养刺激胰岛素分泌，以确定内源性胰岛缺陷是否是对慢性低血糖反应中葡萄糖刺激的胰岛素分泌（GSIS）降低的原因。对照胎儿对亮氨酸和赖氨酸的输注都有反应，动脉血浆胰岛素浓度增加（平均增加：0.13 +/- 0.05 ng / ml亮氨酸; 0.99 +/- 0.26 ng / ml赖氨酸）。慢性（0.37 +/- 0.18 ng / ml）和急性（0.27 +/- 0.19 ng / ml）低血糖会降低体内赖氨酸刺激的胰岛素分泌。急性低血糖后，亮氨酸不刺激胰岛素分泌，但慢性低血糖（0.12 +/- 0.09 ng / ml）可保持亮氨酸。从慢性低血糖胎儿分离出的胰岛具有正常的胰岛素和DNA含量，但在葡萄糖，亮氨酸，精氨酸或赖氨酸刺激下，胰岛素的分数释放降低。来自对照胎儿的分离的胰岛对所有营养物都有反应。因此，慢性晚期低血糖症导致体外营养调节的胰岛素分泌不良，这至少部分负责体内GSIS的降低。慢性低血糖症是人子宫内生长限制（IUGR）的特征，可能导致胰岛缺陷，这是导致人IUGR胎儿和低出生体重婴儿中胰岛素分泌模式减少的原因。

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