EFFECT OF PERTUSSIS TOXIN ON ISLET INSULIN-SECRETION IN OBESE (FA/FA) ZUCKER RATS
EFFECT OF PERTUSSIS TOXIN ON ISLET INSULIN-SECRETION IN OBESE (FA/FA) ZUCKER RATS
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DOI：
10.1016/0303-7207(91)90161-k
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发表时间：
1991-03-01
影响因子：
4.1
通讯作者：
CHAN, CB
中科院分区：
文献类型：
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作者：
CAWTHORN, EG;CHAN, CB
我们使用分离的瘦和肥胖Zucker大鼠的胰岛来确定是否由百日咳毒素敏感的鸟苷酸结合（G（i））蛋白介导的抑制途径有助于肥胖大鼠的高胰岛素血症。 肾上腺素（10（-4）M）和生长抑素（10（-7）M）抑制瘦大鼠和fa/fa大鼠的胰岛素分泌+/- 75%。 用百日咳毒素（300 ng/ml）过夜培养胰岛，在瘦大鼠（+/-120%）中比在肥胖大鼠（+/-60%）中更能增强胰岛素释放。 在瘦大鼠孵育百日咳毒素处理的胰岛与肾上腺素导致较低的免疫反应性胰岛素释放（p = 0.0005）比百日咳毒素处理的胰岛无肾上腺素。 然而，在肥胖大鼠百日咳毒素治疗逆转这种抑制。 百日咳毒素完全逆转生长抑素在两种表型中的抑制作用。 甘丙肽对胰岛素分泌无影响。 细胞cAMP含量在瘦和肥胖大鼠中相似。 抑制激素对cAMP的产生没有影响。 我们的结论是肥胖大鼠的胰岛对胰岛素释放抑制剂的反应正常。 百日咳毒素对生长抑素诱导的抑制作用的恢复表明肥胖大鼠G（i）功能正常。 注意到瘦胰岛和肥胖胰岛对百日咳毒素的敏感性存在细微差异。
We used isolated islets of lean and obese Zucker rats to determine whether inhibitory pathways mediated by pertussis toxin-sensitive guanyl nucleotide-binding (G(i)) proteins contribute to hyperinsulinemia in obese rats. Epinephrine (10(-4) M) and somatostatin (10(-7) M) inhibited insulin secretion by +/- 75% in lean and fa/fa rats. Overnight culture of islets with pertussis toxin (300 ng/ml) enhanced insulin release more in lean (+/- 120%) than obese (+/- 60%) rats. In lean rats incubation of pertussis toxin-treated islets with epinephrine resulted in lower immunoreactive insulin release (p = 0.0005) than pertussis toxin-treated islets without epinephrine. However, in obese rats pertussis toxin treatment reversed this inhibition. Pertussis toxin completely reversed inhibition by somatostatin in both phenotypes. Galanin had no effect on insulin secretion. Cellular cAMP content was similar in lean and obese rats. Inhibitory hormones had no effect on cAMP production. We conclude that islets of obese rats respond normally to inhibitors of insulin release. Reversal of somatostatin-induced inhibition by pertussis toxin indicates normal function of G(i) in obese rats. A subtle difference in sensitivity to pertussis toxin between lean and obese islets was noted.