期刊文献+

高脂诱导BRL-3A细胞胰岛素抵抗模型的建立 被引量:5

Induction of insulin resistance by palmitic acid in BRL-3A cells
下载PDF
导出
摘要 目的:采用棕榈酸(PA)诱导BRL-3A细胞,建立肝细胞胰岛素抵抗体外模型。方法:分别用不同浓度(0、50、100、200、300、400μmol/L)棕榈酸处理BRL-3A细胞不同时间(6、12、24 h)后,检测细胞生存率、基础葡萄糖消耗及胰岛素刺激葡萄糖消耗的变化。结果:高浓度PA(200、300、400μmol/L)使细胞生存率显著降低(P<0.05);低浓度PA(50、100μmol/L)短时间(6和12 h)作用对细胞生存率无明显影响(P>0.05);不同浓度PA短时间(6 h)作用于细胞,其基础葡萄糖消耗及胰岛素刺激葡萄糖消耗与正常组相比无显著变化(P>0.05),作用24 h后细胞葡萄糖消耗量均明显下降(P<0.05),100μmol/L的PA处理12 h可降低细胞基础葡萄糖消耗及胰岛素刺激的葡萄糖消耗量(P<0.05),且在继续培养至72 h摄糖能力无明显改变。结论:100μmol/L的PA作用12 h可诱导BRL-3A细胞产生胰岛素抵抗。 OBJECTIVE:To investigate an insulin resistance in BRL-3A cells after their exposure to palmitic acid(PA).METHODS:BRL-3A cells were incubated with PA(0,50,100,200,300,400 μmol/L) for 6,12 or 24 hours.After the exposure,cell viability,basic and insulin-stimulated glucose consumption were assayed.RESULTS:Incubation of cells with high concentrations of PA(200,300,400 μmol/L) significantly decreased survival of cells(P〈0.05).Incubation of cells with low concentrations of PA(50,100 μmol/L) for 6 and 12 h had no significant effect on cell viability(P〈0.05).The basic and insulin-stimulated glucose consumption in these cells were not altered by different concentration of PA incubation for 6 h(P〉0.05).However,24 h after the exposure,all concentrations of PA decreased glucose consumption(P〈0.05).At 12 h after the exposure,100 μmol/L of PA decreased basic and insulin-stimulated glucose consumption(P〈0.05),and this ability remained unchanged after 72 h of continuing cultured.CONCLUSION:Incubation of BRL-3A cells with 100 μmol/L of PA for 12 h could induce insulin resistance in vitro.
出处 《癌变.畸变.突变》 CAS CSCD 2016年第1期46-50,55,共6页 Carcinogenesis,Teratogenesis & Mutagenesis
基金 国家自然科学基金(31170807)
关键词 棕榈酸 胰岛素抵抗 葡萄糖消耗 葡萄糖氧化酶法 palmitic acid insulin resistance glucose consumption glucose oxidase peroxidase
  • 相关文献

参考文献21

  • 1Reaven GM. Banting lecture 1988 : Role of insulin resistance in humandisease[J]. Diabetes, 1988, 37(12): 1595-1607.
  • 2Chen X, Iqbal N, Boden G. The effects of free fatty acids on gluconeogenesis and glycogenolysis in normal subjects[J]. J Clin Invest, 1999, 103(3): 365-372.
  • 3Tarcin O, Bajaj M, Akalin S. Insulin resistance, adipocyte biology, and thiazolidinediones: a review[J]. Metab Syndr Relat Disord, 2007, 5(2): 103-115.
  • 4Tholen DW, Kroll M, Astles JR, et al. Evaluation of the linearity of quantitative measurement procedures: a statistical approach approved guideline CISI document EP6-A[S]. Wayne, Pa: CLSI, 2003 : 1-60.
  • 5Jacob S, Machann J, Rett K, et al. Association of increased intramyocellular lipid content with insulin resistance in lean nondiabetic offspring of type 2 diabetic subjects[J]. Diabetes, 1999, 48(5): 1113-1119.
  • 6Johannsen DL, Tchoukalova Y, Tam CS, et al. Effect of 8 weeks of overfeeding on ectopic fat deposition and insulin sensitivity: testing the "adipose tissue expandability" hypothesis [J]. Diabetes Care, 2014, 37(10): 2789-2797.
  • 7Masoodi M, Kuda O, Rossmeisl M, et al. Lipid signaling in adipose tissue: Connecting inflammation & metabolism[J]. Biochim Biophys Acta, 2015, 1851(4): 503-518.
  • 8Shulman GI. Ectopic fat in insulin resistance, dyslipidemia, and cardiometabolic disease[J]. N Engl J Med, 2014, 371 (12): 1131-1141.
  • 9Gaggini M, Morelli M, Buzzigoli E, et al. Non-alcoholic fatty liver disease (NAFLD) and its connection with insulin resistance, dyslipidemia, atherosclerosis and coronary heart disease[J].Nutrients, 2013, 5(5): 1544-1560.
  • 10Gruben N, Shiri-Sverdlov R, Koonen DP, et al. Nonalcoholic fatty liver disease: A main driver of insulin resistance or a dangerous liaison?[J]. Biochim Biophys Acta, 2014, 1842 (11): 2329-2343.

二级参考文献16

共引文献24

同被引文献36

引证文献5

二级引证文献17

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