Insulin secretion from ob/ob mouse pancreatic islets: effects of neurotransmitters.
Insulin secretion from ob/ob mouse pancreatic islets: effects of neurotransmitters.
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ob/ob 小鼠胰岛的胰岛素分泌：神经递质的影响。
DOI：
10.1152/ajpendo.1992.262.3.e338
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Romsos,DR
中科院分区：
文献类型：
--
作者：
Tassava,TM;Okuda,T;Romsos,DR
测定了葡萄糖、乙酰胆碱和去甲肾上腺素对 8 至 9 周龄雌性遗传性肥胖 (ob/ob) 和瘦小鼠胰岛胰岛素分泌的影响。 ob/ob胰岛的直径比瘦小鼠胰岛大60%，对葡萄糖的反应分泌的胰岛素多四倍，并且在比瘦小鼠胰岛更低的葡萄糖浓度下分泌胰岛素。在存在 15 mM 葡萄糖的情况下，与瘦胰岛相比，ob/ob 胰岛对乙酰胆碱的反应显示胰岛素分泌绝对增加 8 倍，对去甲肾上腺素抑制反应胰岛素分泌绝对减少 12 倍。在 5 mM 葡萄糖存在下，乙酰胆碱使 ob/ob 胰岛的胰岛素分泌增加三倍，而对瘦胰岛没有影响。当ob/ob和瘦胰岛都受到葡萄糖刺激达到同等水平的胰岛素分泌时，乙酰胆碱在ob/ob和瘦胰岛中同等地增强葡萄糖诱导的胰岛素分泌。因此，ob/ob 胰岛的葡萄糖诱导的反应性增强可以解释与瘦胰岛相比，ob/ob 胰岛中胰岛素分泌的乙酰胆碱增强作用更大，并且可能解释去甲肾上腺素对胰岛素分泌的抑制更大。这些数据与以下假设一致：ob/ob 小鼠胰岛的主要改变是葡萄糖敏感性和反应性，这随后增加了 ob/ob 胰岛对胰岛素分泌的神经调节的敏感性。
Effects of glucose, acetylcholine, and norepinephrine on insulin secretion from pancreatic islets of 8- to 9-wk-old female genetically obese (ob/ob) and lean mice were determined. The ob/ob islets were 60% larger in diameter than lean mouse islets, secreted fourfold more insulin in response to glucose, and secreted insulin at lower glucose concentrations than lean islets. In the presence of 15 mM glucose, ob/ob islets showed an 8-fold greater absolute increase in insulin secretion in response to acetylcholine and a 12-fold greater absolute decrease in insulin secretion in response to norepinephrine inhibition compared with lean islets. In the presence of 5 mM glucose, acetylcholine increased insulin secretion by threefold from ob/ob islets with no effect on lean islets. When both ob/ob and lean islets were stimulated by glucose to equivalent levels of insulin secretion, acetylcholine potentiated glucose-induced insulin secretion equally in ob/ob and lean islets. Enhanced glucose-induced responsiveness of ob/ob islets thus can explain the greater acetylcholine potentiation of insulin secretion and probably the greater norepinephrine inhibition of insulin secretion in ob/ob islets compared with lean islets. These data are consistent with the hypotheses that the major alteration in ob/ob mouse islets is in glucose sensitivity and responsiveness, which subsequently increases ob/ob islet susceptibility to neural regulation of insulin secretion.
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