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目的通过脂蛋白脂肪酶(LPL)基因敲除杂合子(LPL~(+/-))小鼠糖脂代谢研究,了解脂毒性在糖代谢中的作用。方法正常对照C57小鼠(16周龄)、LPL~(+/-)小鼠(16周龄)、LPL~(+/-)小鼠(28周龄)各6只,测血清脂质水平,腹腔葡萄糖耐量实验评价胰岛素抵抗(IR)及β细胞功能,同时检测肝脏、骨骼肌、胰腺组织内脂质水平。结果 (1)LPL~(+/-)16周龄组小鼠内脏脂肪质量较对照组显著增加(P<0.05)。LPL~(-/-)16周龄组与LPL~(+/-)28周龄组之间肝脏TG、内脏脂肪和皮下脂肪的质量和含量的变化差异有统计学意义(P<0.05)。与对照组相比,LPL~(+/-)28周龄组血清TG、肝脏TG,及肝脏、骨骼肌、胰腺游离脂肪酸(FFA)水平显著升高(P<0.05)。(2)LPL~(+/-)16周龄组小鼠FBG、血糖曲线下面积(AUC_G)、空腹胰岛素(FIns)、HOMA-β-HOMA-IR均高于对照组,但差异无统计学意义。LPL~(+/-)28周龄组小鼠FBG、AUC_G、FIns、HOMA-β、HOMA-IR较LPL~(+/-) 16周龄组高,且FIns、HOMA-IR的增高有统计学意义(P<0.05)。LPL~(+/-)28周龄组与对照组间AUC_G、FIns、HOMA-IR的变化有统计学意义(P<0.05)。结论 LPL~(+/-)引起脂代谢异常,并随着周龄的延长,脂代谢异常逐渐加重;同时出现了糖代谢异常。
OBJECTIVE: To investigate the role of lipotoxicity in glucose metabolism in lipopolysaccharide (LPL) knockout heterozygotes (LPL ~ (+/-)) mice. Methods Normal control C57 mice (16 weeks old), LPL +/- mice (16 weeks old) and LPL +/- mice (28 weeks old) each had 6 serum lipid levels , Intraperitoneal glucose tolerance test to evaluate insulin resistance (IR) and β-cell function, and to detect lipid levels in liver, skeletal muscle and pancreas at the same time. Results (1) The visceral fat mass of mice in LPL +/- 16 weeks group was significantly higher than that in control group (P <0.05). There were significant differences in the contents of TG, visceral fat and subcutaneous fat between 16-week-old LPL group and 28-week old LPL group (P <0.05). Compared with the control group, serum TG, liver TG, hepatic, skeletal muscle and free fatty acid (FFA) in the LPL +/- 28 weeks group were significantly increased (P <0.05). (2) FBG, area under the curve of blood glucose (AUC_G), FIns and HOMA-β-HOMA-IR of mice in LPL +/- 16 weeks group were higher than those in control group, but the difference was not statistically significant significance. The FBG, AUC_G, FIns, HOMA-β and HOMA-IR in 28-week-old LPL +/- mice were higher than those in 16-week old LPL +/- mice, and the statistic of FIns and HOMA- Significance (P <0.05). The changes of AUC_G, FIns and HOMA-IR between the 28-week-old LPL +/- group and the control group were statistically significant (P <0.05). Conclusions LPL ~ (+/-) induced abnormal lipid metabolism. With the increase of age, the abnormal lipid metabolism gradually aggravated. At the same time, abnormal glucose metabolism occurred.