期刊文献+

甘精胰岛素对游离脂肪酸诱导的RIN-m细胞凋亡的影响 被引量:28

Effects of Insulin Glargine on FFA-induced Apoptosis in RIN-m Cells
暂未订购
导出
摘要 【目的】研究甘精胰岛素(insulinglargine)对游离脂肪酸诱导的β细胞凋亡是否具有保护作用。【方法】不同浓度的甘精胰岛素、普通人胰岛素以及IGF-1与0.3mmol/L棕榈酸分别加入RIN-m细胞培养液中,24h后,采用Hoechst33342染色、流式细胞仪以及ELISA方法检测RIN-m细胞的凋亡。【结果】0.3mmol/L棕榈酸诱导RIN-m细胞凋亡率达42.10%±4.24%,同时加入甘精胰岛素或者普通胰岛素(均为100nmol/L)的凋亡率分别为32.00%±3.08%和35.97%±3.14%,甘精胰岛素对凋亡的抑制作用明显强于普通胰岛素,并呈剂量依赖性。【结论】甘精胰岛素对游离脂肪酸诱导的β细胞凋亡具有呈剂量依赖性的保护作用。 [Objective]To investigate the effects of insulin glargine on apoptosis induced by free fatty acid in pancreatic βcells. [Methods] Apoptosis was determined by Hoechst staining, flow cytometry, and ELISA kit in RIN-m cells incubated by palmitic acid (0.3mmol/L) for 24 hours in the absence or presence of insulin glargine, regular insulin or IGF-1 at various dosages. [Results] The percentages of SubG1 cells in palmitic acid-treated control group, glargine treated group, and regular insulin-treated group were 42.10%±4.24%, 32.00%±3.08%, and 35.97%±3.14%, respectively. The anti-apoptotic effect of insulin glargine was dose-dependent and stronger than regular insulin at all corresponding dosage. [Conclusion] Insulin glargine can dose-dependently protect apoptosis induced by free fatty acid in pancreaticβcells.
出处 《中山大学学报(医学科学版)》 CAS CSCD 北大核心 2005年第4期413-416,共4页 Journal of Sun Yat-Sen University:Medical Sciences
基金 广东省社会发展重点攻关项目(2002C30503)
  • 相关文献

参考文献12

  • 1Kurtzhals P, Schaffer L, Sorensen A, et al. Correlations of receptor binding and metabolic and mitogenic potencies of insulin analogs designed for clinical use[J]. Diabetes, 2000, 49(6):999-1005.
  • 2Rakatzi I, Seipke G, Eckel J. [LysB3,GluB29 ]insulin:a novel insulin analog with enhanced b cell protective action [J]. Biochem Biophys Res Commun, 2003, 310(3):852-59.
  • 3Zhou YP, Grill VE. Long-term exposure of rat pancreatic islets to fatty acids inhibits glucose-induced insulin secretion and biosynthesis through a glucose fatty acid cycle[J]. J Clin Invest, 1994, 93(2):870-76.
  • 4Gerich JE. Contributions of insulin-resistance and insulin-secretory defects to the pathogenesis of type 2diabetes mellitus [J]. Mayo Clin Proc, 2003, 78(4):447-56.
  • 5Kahn SE. The importance of the β-cell in the pathogenesis of type 2 diabetes mellitus [J]. Am J Med,2000, 108(suppl 6a):2S-8S.
  • 6Butler AE, Janson J, Bonner-Weir S, et al. Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes [J]. Diabetes, 2003, 52(1):102-10.
  • 7Butler AE, Janson J, Soeller WC, et al. Increased beta-cell apoptosis prevents adaptive increase in betacell mass in mouse model of type 2 diabetes: evidence for role of islet amyloid formation rather than direct action of amyloid [J]. Diabetes, 2003, 52(9):2304-14.
  • 8Mandrup-Poulsen T. Apoptotic signal transduction pathways in diabetes [J]. Biochem Pharmacol, 2003, 66(8): 1433-40.
  • 9Robertson RP, Harmon J, Tran PO, et al. β-cell glucose toxicity, lipotoxicity, and chronic oxidative stress in type 2 diabetes [J]. Diabetes, 2004, 53 (Suppl1):S119 - 24.
  • 10Peruzzi F, Prisco M, Dews M, et al. Pleiotropic effects of fatty acids on pancreatic β-cells [J]. J Cell Physiol,2002, 194 (1):1 - 12.

同被引文献195

引证文献28

二级引证文献137

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部