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1
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2
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3
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4
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Venom-Derived Peptides Inhibiting Voltage-Gated Sodium and Calcium Channels in Mammalian Sensory Neurons.来源于毒液的肽类物质可抑制哺乳动物感觉神经元中的电压门控钠离子和钙离子通道。
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本文引用的文献

1
The Na+ -Ca2+ exchanger is essential for embryonic heart development in mice.钠钙交换体对小鼠胚胎心脏发育至关重要。
Mol Cells. 2000 Dec 31;10(6):712-22. doi: 10.1007/s10059-000-0712-2.
2
Understanding the pathogenesis and treatment of insulin resistance and type 2 diabetes mellitus: what can we learn from transgenic and knockout mice?了解胰岛素抵抗和2型糖尿病的发病机制及治疗方法：我们能从转基因和基因敲除小鼠中学到什么？
Diabetes Metab. 2000 Dec;26(6):433-48.
3
Minireview: the glucagon-like peptides.小型综述：胰高血糖素样肽
Endocrinology. 2001 Feb;142(2):521-7. doi: 10.1210/endo.142.2.7983.
4
Intercellular signals regulating pancreas development and function.调节胰腺发育和功能的细胞间信号。
Genes Dev. 2001 Jan 15;15(2):111-27. doi: 10.1101/gad.859401.
5
Attenuation of FGF signalling in mouse beta-cells leads to diabetes.小鼠β细胞中FGF信号的减弱会导致糖尿病。
Nature. 2000 Dec 14;408(6814):864-8. doi: 10.1038/35048589.
6
Impaired insulin secretion and increased insulin sensitivity in familial maturity-onset diabetes of the young 4 (insulin promoter factor 1 gene).年轻的成年发病型糖尿病4型（胰岛素启动因子1基因）中胰岛素分泌受损及胰岛素敏感性增加。
Diabetes. 2000 Nov;49(11):1856-64. doi: 10.2337/diabetes.49.11.1856.
7
Increased insulin sensitivity and decreased insulin secretion in offspring of insulin-sensitive type 2 diabetic patients.胰岛素敏感型2型糖尿病患者后代的胰岛素敏感性增加及胰岛素分泌减少。
Metabolism. 2000 Sep;49(9):1219-23. doi: 10.1053/meta.2000.8623.
8
Congenital deafness and sinoatrial node dysfunction in mice lacking class D L-type Ca2+ channels.缺乏D类L型钙离子通道的小鼠出现先天性耳聋和窦房结功能障碍。
Cell. 2000 Jul 7;102(1):89-97. doi: 10.1016/s0092-8674(00)00013-1.
9
Activin receptor patterning of foregut organogenesis.前肠器官发生中的激活素受体模式形成
Genes Dev. 2000 Aug 1;14(15):1866-71.
10
Genetic modifiers of the insulin resistance phenotype in mice.小鼠胰岛素抵抗表型的遗传修饰因子。
Diabetes. 2000 Apr;49(4):589-96. doi: 10.2337/diabetes.49.4.589.

出生后胰腺β细胞生成中L型Ca(2+)通道α(1D)亚基的需求。

Requirement for the L-type Ca(2+) channel alpha(1D) subunit in postnatal pancreatic beta cell generation.

作者信息

Namkung Y, Skrypnyk N, Jeong M J, Lee T, Lee M S, Kim H L, Chin H, Suh P G, Kim S S, Shin H S

机构信息

National Creative Research Initiatives Center for Calcium and Learning, Pohang University of Science and Technology, Pohang, Korea.

出版信息

J Clin Invest. 2001 Oct;108(7):1015-22. doi: 10.1172/JCI13310.

DOI:10.1172/JCI13310
PMID:11581302
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC200955/
Abstract

Pancreatic beta cells are the source of insulin, which directly lowers blood glucose levels in the body. Our analyses of alpha(1D) gene-knockout (alpha(1D)(-/-)) mice show that the L-type calcium channel, alpha(1D), is required for proper beta cell generation in the postnatal pancreas. Knockout mice were characteristically slightly smaller than their littermates and exhibited hypoinsulinemia and glucose intolerance. However, isolated alpha(1D)(-/-) islets persisted in glucose sensing and insulin secretion, with compensatory overexpression of another L-type channel gene, alpha(1C). Histologically, newborn alpha(1D)(-/-) mice had an equivalent number of islets to wild-type mice. In contrast, adult alpha(1D)(-/-) mice showed a decrease in the number and size of islets, compared with littermate wild-type mice due to a decrease in beta cell generation. TUNEL staining showed that there was no increase in cell death in alpha(1D)(-/-) islets, and a 5-bromo-2' deoxyuridine-labeling (BrdU-labeling) assay illustrated significant reduction in the proliferation rate of beta cells in alpha(1D)(-/-) islets.

摘要

胰腺β细胞是胰岛素的来源，胰岛素可直接降低体内血糖水平。我们对α（1D）基因敲除（α（1D）-/-）小鼠的分析表明，L型钙通道α（1D）是出生后胰腺中β细胞正常生成所必需的。基因敲除小鼠的特征是比同窝小鼠略小，表现出低胰岛素血症和葡萄糖不耐受。然而，分离出的α（1D）-/-胰岛仍具有葡萄糖感应和胰岛素分泌功能，另一个L型通道基因α（1C）出现代偿性过表达。组织学上，新生α（1D）-/-小鼠的胰岛数量与野生型小鼠相当。相比之下，成年α（1D）-/-小鼠与同窝野生型小鼠相比，胰岛数量和大小减少，这是由于β细胞生成减少所致。TUNEL染色显示α（1D）-/-胰岛中的细胞死亡没有增加，5-溴-2'-脱氧尿苷标记（BrdU标记）试验表明α（1D）-/-胰岛中β细胞的增殖率显著降低。