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葡萄糖刺激下大鼠胰岛磷脂之间的相互关系及其对培养基中肌醇和丁卡因的反应。

Inter-relations between the phospholipids of rat pancreatic islets during glucose stimulation, and their response to medium inositol and tetracaine.

作者信息

Freinkel N, El Younsi C, Dawson M C

出版信息

Eur J Biochem. 1975 Nov 1;59(1):245-52. doi: 10.1111/j.1432-1033.1975.tb02448.x.

Abstract
  1. Isolated rat pancreatic islets subjected to an increase in glucose concentration from 0.5 to 3 mg/ml showed an increased insulin secretion and 32P-labelling of their phospholipids, especially of phosphatidylinositol, phosphatidylethanolamine, phosphatidylglycerol, and CDP diglyceride. Neither fructose or inositol produced a similar effect. 2. The enhanced labelling of CDP diglyceride and phosphatidylglycerol was suppressed by adding inositol (0.1 mg/ml), while the phosphatidylinositol labelling was increased still further. 3. Tetracaine (0.5 mM), an antagonist of insulin secretion, inhi-ited phosphatidylinositol synthesis while phosphatidylglycerol, CDP diglyceride and phosphatidic acid formation were markedly increased. These effects on phospholipid synthesis were substantially reversed by adding inositol to the medium. Tetracaine also prevented the catabolism of phosphatidylinositol in prelabelled islets but this inhibiton was not reversed by inositol. 4. Inositol addition did not affect insulin secretion in glucose-stimulated islets nor secretion in tetracaine-treated islets. This need not exclude a possible role for heightened phosphatidylinositol cleavage in stimulated insulin secretion.
摘要
  1. 将分离的大鼠胰岛置于葡萄糖浓度从0.5毫克/毫升升至3毫克/毫升的环境中,其胰岛素分泌增加,磷脂(尤其是磷脂酰肌醇、磷脂酰乙醇胺、磷脂酰甘油和CDP甘油二酯)的32P标记增加。果糖或肌醇均未产生类似效果。2. 添加肌醇(0.1毫克/毫升)可抑制CDP甘油二酯和磷脂酰甘油标记的增强,而磷脂酰肌醇标记进一步增加。3. 胰岛素分泌拮抗剂丁卡因(0.5毫摩尔)抑制磷脂酰肌醇合成,而磷脂酰甘油、CDP甘油二酯和磷脂酸的形成则显著增加。向培养基中添加肌醇可基本逆转这些对磷脂合成的影响。丁卡因还可阻止预先标记的胰岛中磷脂酰肌醇的分解代谢,但这种抑制作用不能被肌醇逆转。4. 添加肌醇不影响葡萄糖刺激的胰岛中的胰岛素分泌,也不影响丁卡因处理的胰岛中的分泌。这并不排除增强的磷脂酰肌醇裂解在刺激胰岛素分泌中可能发挥的作用。

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