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二氮嗪诱导的长期高血糖症。I. B细胞胰岛素释放能力的保留。

Diazoxide-induced long-term hyperglycemia. I. Preservation of B-cell insulin-releasing capacity.

作者信息

Gomis R, Plaza C, Malaisse W J

机构信息

Endocrinology and Diabetes Unit, Hospital Clinic, Barcelona, Spain.

出版信息

Diabetes Res. 1988 Dec;9(4):183-6.

PMID:3073904
Abstract

Although several models of experimental diabetes mellitus are currently available, none of them appears to be optimally suited to study the possible deleterious effect of sustained hyperglycemia upon biochemical and functional variables in pancreatic islet cells in the absence of chronic stimulation of secretory activity. In the present study, oral diazoxide administration (0.33 g/Kg body wt. thrice per day for three days) to rats was used to cause both hypoinsulinemia and hyperglycemia (greater than or equal to 10.0 mM), the latter persisting, albeit at a somewhat lower level, for at least 1-2 days after cessation of diazoxide treatment. Ten hours after the last administration of diazoxide, the secretory response of isolated islets to D-glucose over 90 min incubation was not impaired. It is proposed that such a model may help to dissociate the influence of hyperglycemia itself upon islet cell behaviour from the consequences of sustained hypersecretion of insulin.

摘要

尽管目前有几种实验性糖尿病模型,但似乎没有一种最适合在不长期刺激分泌活动的情况下,研究持续高血糖对胰岛细胞生化和功能变量可能产生的有害影响。在本研究中,给大鼠口服二氮嗪(0.33 g/Kg体重,每天三次,共三天),以引起低胰岛素血症和高血糖(大于或等于10.0 mM),后者在二氮嗪治疗停止后至少持续1-2天,尽管水平有所降低。在最后一次给予二氮嗪10小时后,分离的胰岛在90分钟孵育期间对D-葡萄糖的分泌反应未受损。有人提出,这样的模型可能有助于将高血糖本身对胰岛细胞行为的影响与胰岛素持续高分泌的后果区分开来。

相似文献

1
Diazoxide-induced long-term hyperglycemia. I. Preservation of B-cell insulin-releasing capacity.二氮嗪诱导的长期高血糖症。I. B细胞胰岛素释放能力的保留。
Diabetes Res. 1988 Dec;9(4):183-6.
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Diazoxide-induced long-term hyperglycemia. II. Slackening of proinsulin conversion.
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Diazoxide unmasks glucose inhibition of insulin release by counteracting entry of Ca2+.二氮嗪通过抵消钙离子内流来消除葡萄糖对胰岛素释放的抑制作用。
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Diazoxide attenuates glucose-induced defects in first-phase insulin release and pulsatile insulin secretion in human islets.二氮嗪可减轻葡萄糖诱导的人类胰岛中第一相胰岛素释放和胰岛素脉冲分泌的缺陷。
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Diazoxide infusion at excess but not at basal hyperglycemia enhances beta-cell sensitivity to glucose in vitro in neonatally streptozotocin-diabetic rats.在新生期经链脲佐菌素诱导糖尿病的大鼠中,过量而非基础高血糖状态下输注二氮嗪可增强体外培养的β细胞对葡萄糖的敏感性。
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Further studies on diazoxide suppression of insulin release from abnormal and normal islet tissue in man.关于二氮嗪对人体异常及正常胰岛组织胰岛素释放抑制作用的进一步研究。
Ann N Y Acad Sci. 1968 Apr 11;150(2):261-80. doi: 10.1111/j.1749-6632.1968.tb19051.x.
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Biochemical aspects of the hyperglycemic action of diazoxide.
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Impact of uncoupling glucose stimulus from secretion on B-cell release and biosynthesis.将葡萄糖刺激与分泌解偶联对β细胞释放和生物合成的影响。
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Am J Physiol Endocrinol Metab. 2006 Jan;290(1):E26-E33. doi: 10.1152/ajpendo.00149.2005. Epub 2005 Aug 16.

引用本文的文献

1
Paradoxical inhibition of insulin secretion by glucose in non-insulin-dependent diabetic patients.非胰岛素依赖型糖尿病患者中葡萄糖对胰岛素分泌的反常抑制作用。
Acta Diabetol. 1995 Mar;32(1):1-6. doi: 10.1007/BF00581036.