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胰淀素对大鼠胰岛素分泌的影响及其机理的探讨 被引量:9

Effect of amylin on insulin secretion in rat pancreatic islets and its mechanism
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摘要 目的 为研究胰淀素( Amylin) 对大鼠胰岛细胞分泌胰岛素的影响和机理。方法 用放免和荧光方法分别检测经不同浓度胰淀素温育的大鼠胰岛细胞的胰岛素分泌量、细胞内 Ca 《及c A M P 含量。结果 在胰淀素10μmol/ L 组中高糖刺激下的胰岛素含量、细胞内 Ca 《含量,细胞内c A M P 含量分别为0 .89 ±0 .21ng/ ml、63 ±10nmol/ L、29 .3 ±3 .3pmol/1 ×106 细胞与对照组(1 .75 ±0 .42ng/ml、135 ±10n mol/ L、36 .3 ±7 .4pmol/ L) 比较,其中胰岛素分泌量、细胞内 Ca 《含量均明显降低, P< 0 .01 ,细胞内c A M P 含量有减少趋势。结论 高浓度的胰淀素抑制了胰岛细胞内 Ca 《升高和/ 或细胞内c A M P 形成,可能是胰岛素分泌减少的原因之一。 Objective To study the effect of Amylin on insulin secretion in rat pancreatic islet cells and its mechanism. Methods Radio immunological and fluorescence methods were used to determine the amount of insulin secretion as well as content of intracellular Ca and cAMP by the rat islet cells incubated with amylin in different concentrations. Results In the 10μM/L amylin group, the glucose stimulated insulin release volume, intracellular Ca and cAMP content were 0.89±0.21ng/ml, 63±10nmol/L and 29.3±3.3pmol/1×10 6 cell respectively as compared with the control group (1.75±0.41ng/ml, 135±10nmol/L and 36.3±7.4 pmol/1×10 6 cells respectively). The insulin release volume and intracellular Ca decreased remarkably (P<0.01), while cAMP content had a tendency to decrease. Conclusion High concentration of amylin is responsible for the prevention of rise of Ca inside the islet B cells and /or the decrease of cAMP content which is one of the causes that bring about the decreased release of insulin.
出处 《中华内分泌代谢杂志》 CAS CSCD 北大核心 1998年第3期186-189,共4页 Chinese Journal of Endocrinology and Metabolism
关键词 胰淀素 胰岛系 钙离子 环磷酸腺苷 胰岛细胞 Amylin Insulin Ca cAMP
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  • 1钱玉宁,中国糖尿病杂志,1993年,1期,21页

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  • 1Marshak S, Leibowitz G, Bertuzzi F, Socci C, Kaiser N, Gross D J, Cerasi E, MeUoul D. Impaired beta-cell cell functions induced by chronic exposure of cultured human pancreatic islets to high glucose. Diabetes, 1999,48 (6): 1230-1236
  • 2Misler S, Barnett DW, Pressel DM, Gillis KD, Scharp DW, Falke LC. Stimulus-secretion coupling in beta-cells of transplantable human islets of langerhans: evidence for a critical role for Ca^2+ entry. Diabetes, 1992, 41(6): 662-670
  • 3Ashcroft FM, Kelly RP, Smith PA. Two types of Ca channel in rat pancreatic beta-cells. Pflugers Arch, 1990,415 (4): 504-506
  • 4Polonsky KS. Lilly Lecture 1994. The beta-cell in diabetes: from molecular genetics to clinical research. Diabetes, 1995, 44(6):705-717
  • 5Misler S, Barnett DW, Gillis KD, Pressel DM. Electrophysiology of stimulus-secretion coupling in human beta-cells. Diabetes, 1992,41(10):1221-1228
  • 6Ashcroft FM, Proks P, Smith PA, Ammala C, Bokvist K, Rorsman P. Stimulus-secretion coupling in pancreatic beta cells. J Cell Biochem, 1994,55(suppl):54-65
  • 7Taguchi N, Aizawa T, Sato Y, Ishihara F, Hashizume K. Mechanism of glucose-induded biphasic insulin release: physiological role of adenosine triphosphate-sensitive K^+ channel-independent glucose action. Endocrinology, 1995, 136(9):3942-3948
  • 8Roe MW, Lancaster ME, Mertz RJ, Worley JF 3rd, Dukes ID. Voltage-dependent intracellular calcium release from mouse islets stimulated by glucose. J Biol chem, 1993, 268(14):9953-9956
  • 9Robertson RP. Chronic oxidative stress as a central mechanism for glucose toxicity in pancreatic islet beta ceils in diabetes. J Biol Chem, 2004,279(41):42351-42354
  • 10Buffer AE, Janson J, Soeller WC, et al, Increased beta-cell apoptosis prevents adaptive increase in beta-cell mass in mouse model of type 2 diabetes: evidence for role of islet amyloid formation rather than direct action of amyloid. Diabetes, 2003, 52: 2304-2314.

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