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葡萄糖加茶碱刺激的胰岛素分泌的第一阶段以及生长抑素在遗传性糖尿病小鼠(C57BL/KsJ-mdb)中的抑制作用。

First phase of insulin secretion stimulated by glucose plus theophylline and inhibitory effect of somatostatin in genetically diabetic mice (C57BL/KsJ-mdb).

作者信息

Karabatas L M, Arata M, Anaya L, Cresto J C, Pivetta O H, Basabe J C

机构信息

Fundación Laboratorio de Investigaciones Pediátricas, Buenos Aires, Argentina.

出版信息

Diabetologia. 1988 Jun;31(6):375-8. doi: 10.1007/BF02341506.

DOI:10.1007/BF02341506
PMID:2901377
Abstract

In a previous study in C57BL/KsJ mdb/mdb mice aged 4 to 12 days we observed a diminished first phase of glucose-induced insulin secretion in vitro, and alterations in the inhibitory effect of somatostatin on insulin secretion. This study explores, using perifused pancreatic slices, whether the reduced B-cell responsiveness to somatostatin in mdb/mdb mice can be overcome upon induction of a biphasic insulin release by using theophylline. Under these conditions our results show: (1) in mdb/mdb mice aged 4 to 6 days, the restoration of the first peak of insulin secretion overcomes the reduced B-cell sensitivity to somatostatin; and (2) in mdb/mdb mice aged 7 to 12 days, the addition of theophylline only causes a partial restoration of B-cell responsiveness to somatostatin, suggesting that other mechanisms could be involved in the progressive impairement of B-cell sensitivity to somatostatin inhibitory effect.

摘要

在先前一项针对4至12日龄C57BL/KsJ mdb/mdb小鼠的研究中,我们观察到体外葡萄糖诱导的胰岛素分泌的第一阶段有所减少,以及生长抑素对胰岛素分泌的抑制作用发生改变。本研究使用灌流胰腺切片,探究在通过茶碱诱导双相胰岛素释放时,mdb/mdb小鼠中B细胞对生长抑素反应性降低的情况是否能够得到克服。在这些条件下,我们的结果显示:(1)在4至6日龄的mdb/mdb小鼠中,胰岛素分泌第一个峰值的恢复克服了B细胞对生长抑素敏感性的降低;(2)在7至12日龄的mdb/mdb小鼠中,添加茶碱仅使B细胞对生长抑素的反应性部分恢复,这表明其他机制可能参与了B细胞对生长抑素抑制作用敏感性的逐渐受损。

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1
First phase of insulin secretion stimulated by glucose plus theophylline and inhibitory effect of somatostatin in genetically diabetic mice (C57BL/KsJ-mdb).葡萄糖加茶碱刺激的胰岛素分泌的第一阶段以及生长抑素在遗传性糖尿病小鼠(C57BL/KsJ-mdb)中的抑制作用。
Diabetologia. 1988 Jun;31(6):375-8. doi: 10.1007/BF02341506.
2
Secretion and effect of somatostatin in early stages of the diabetic syndrome in C57BL/KsJ-mdb mice.生长抑素在C57BL/KsJ-mdb小鼠糖尿病综合征早期的分泌及作用
Diabetologia. 1986 Aug;29(8):485-8. doi: 10.1007/BF00453498.
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Insulin secretion induced by alloantigens. Mechanisms of action.同种异体抗原诱导的胰岛素分泌。作用机制。
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本文引用的文献

1
A temporal study of somatostatin secretion and its inhibitory effect in genetically diabetic mice (C57BL/KsJ-db/db).对遗传性糖尿病小鼠(C57BL/KsJ-db/db)生长抑素分泌及其抑制作用的时间研究。
Endocrinology. 1983 Dec;113(6):1927-34. doi: 10.1210/endo-113-6-1927.
2
Role of the secretion vesicle in the transport of receptors: modulation of somatostatin binding to pancreatic islets.分泌囊泡在受体转运中的作用:生长抑素与胰岛结合的调节。
Endocrinology. 1982 Jul;111(1):316-23. doi: 10.1210/endo-111-1-316.
3
Coated charcoal immunoassay of insulin.
胰岛素的包被炭免疫测定法。
J Clin Endocrinol Metab. 1965 Oct;25(10):1375-84. doi: 10.1210/jcem-25-10-1375.
4
Studies with the mutation, diabetes, in the mouse.对小鼠糖尿病突变的研究。
Diabetologia. 1967 Apr;3(2):238-48. doi: 10.1007/BF01222201.
5
[Regulation of insulin release in perifused pancreatic tissue].[灌注外周胰腺组织中胰岛素释放的调节]
Acta Diabetol Lat. 1969 Sep;6 Suppl 1:580-96.
6
Insulin radioimmunoassay by the charcoal-dextran technique.采用活性炭-葡聚糖技术的胰岛素放射免疫测定法。
Diabetologia. 1972 Aug;8(4):292-5. doi: 10.1007/BF01225574.
7
The influence of genetic background on expression of mutations at the diabetes locus in the mouse. I. C57BL-KsJ and C57BL-6J strains.遗传背景对小鼠糖尿病位点突变表达的影响。I. C57BL-KsJ和C57BL-6J品系。
Biochem Genet. 1972 Aug;7(1):1-13. doi: 10.1007/BF00487005.
8
The role of adenosine 3':5'-cyclic monophosphate in the regulation of insulin release. Properties of islet-cell adenosine 3':5'-cyclic monophosphate phosphodiesterase.3':5'-环磷酸腺苷在胰岛素释放调节中的作用。胰岛细胞3':5'-环磷酸腺苷磷酸二酯酶的特性。
Biochem J. 1972 Oct;129(4):945-52. doi: 10.1042/bj1290945.
9
A possible role for the adenylcyclase system in insulin secretion.腺苷酸环化酶系统在胰岛素分泌中的可能作用。
J Clin Invest. 1967 Nov;46(11):1724-34. doi: 10.1172/JCI105663.
10
Secretion and effect of somatostatin in early stages of the diabetic syndrome in C57BL/KsJ-mdb mice.生长抑素在C57BL/KsJ-mdb小鼠糖尿病综合征早期的分泌及作用
Diabetologia. 1986 Aug;29(8):485-8. doi: 10.1007/BF00453498.