Cui Wei, Huang Ting, Liu Jun-li, Shi Bing-yin
Department of Endocrinology, the First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2009 Mar;25(3):219-21.
To investigate the effect of saturated fatty acid palmitate (PA) on cell viability of MIN6 beta-cell and the possible cell cycle pathways affected by PA.
MIN6 cells were synchronized at G(0); phase by serum deprivation for 36 h, and further MIN6 cells were exposed to different concentrations of PA(0.25-1.0 mmol/L, 45 min-24 h)compared with control cell treated with BSA.Cell viability was assessed by MTT colorimetric assay. The cell cycle was measured by FACS analysis, and cell cycle proteins were further detected using Western blot.
(1)PA significantly affected the cell viability of MIN6 cells. (2)The G(0);/G(1); cell cycle arrest (n=6, P<0.05) also induced by PA, whereas MIN6 cells in S and G(2);/M phase were decreased. (3) For cell cycle proteins, PA treatment caused significant reductions in cyclin D1 and CDK4 levels, which was consistent to the cell cycle delay.
The findings thus suggest that increased PA directly affects pancreatic beta-cell proliferation, possibly by reducing the levels of cyclin D1/CDK4 in the cells, which results in arresting in progression through the G(1); phase to the S phase of the cell cycle.
研究饱和脂肪酸棕榈酸酯（PA）对MIN6β细胞活力的影响以及PA可能影响的细胞周期途径。
通过血清饥饿36小时使MIN6细胞同步于G(0)期，与用牛血清白蛋白处理的对照细胞相比，将MIN6细胞进一步暴露于不同浓度的PA（0.25 - 1.0 mmol/L，45分钟 - 24小时）。通过MTT比色法评估细胞活力。通过流式细胞术分析测量细胞周期，并使用蛋白质印迹法进一步检测细胞周期蛋白。
（1）PA显著影响MIN6细胞的活力。（2）PA还诱导G(0)/G(1)细胞周期阻滞（n = 6，P < 0.05），而处于S期和G(2)/M期的MIN6细胞减少。（3）对于细胞周期蛋白，PA处理导致细胞周期蛋白D1和细胞周期蛋白依赖性激酶4水平显著降低，这与细胞周期延迟一致。
因此，研究结果表明，PA增加直接影响胰腺β细胞增殖，可能是通过降低细胞中细胞周期蛋白D1/细胞周期蛋白依赖性激酶4的水平，从而导致细胞周期从G(1)期进展到S期受阻。
