| 秦苗 王文递 王明亮 宋彬妤 吴惠文△.代谢性内毒素血症在果糖诱发的NAFLD等代谢疾病中的作用研究[J].,2016,16(33):6440-6444 |
| 代谢性内毒素血症在果糖诱发的NAFLD等代谢疾病中的作用研究 |
| The Studies about the Role of Metabolic Endotoxemia in Fructose inducedNAFLD Metabolic Diseases |
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| DOI： |
| 中文关键词: 内毒素血症 非酒精性脂肪性肝病 胰岛素抵抗 炎症 |
| 英文关键词: Endotoxemia Nonalcoholic fatty liver disease Insulin resistance Inflammatory |
| 基金项目:山西省研究生优秀创新项目（20103052） |
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| 中文摘要: |
| 目的：探讨果糖饮食诱发大鼠发生非酒精性脂肪性肝病（NAFLD）等代谢疾病中，代谢性内毒素血症发挥的作用及机制。
方法：30只SD雄性大鼠随机分为三组：正常对照组（NC组）、高果糖组(HFD组，8%高果糖水喂养)、内毒素组（LPS组, 300 ug·kg-1·d-1
皮下注射）。8 周糖耐量实验后，测定血浆内毒素(LPS)、胰岛素、血脂系列，计算胰岛素抵抗指数（HOMA-IR），检测促炎因子
（TNF-alpha、IL-6）表达，观测肝组织病理学变化，Western blot 检测肝组织胰岛素信号转导关键蛋白、内毒素受体表达。结果：与NC组
比较，HFD 组与LPS 组大鼠血浆LPS、血脂（TG、TC、FFA、HDL）、促炎因子（TNF-alpha、IL-6），FPG(Fasting plasm glucose)、FINS(Fasting
insulin)、HOME-IR (homeostasis model assessment of IR) 的水平有统计学意义（P＜0.05，P＜0.01），胰岛素受体底物
P-IRS1Tyr632/IRS1 比值下降、内毒素受体TLR-4 表达升高（P＜0.05，P＜0.01），HFD 组与LPS组上述指标变化无统计学差异。结
论：高果糖饮食及皮下注射LPS诱发大鼠发生NAFLD 等代谢疾病时，普遍伴有内毒素血症；LPS 通过炎症机制引发胰岛素抵抗，
促进NAFLD 等代谢疾病的发生发展。 |
| 英文摘要: |
| Objective:To investigate the role and mechanismof metabolic endotoxemia in fructose diet induced NAFLDmetabolic
diseases of rats.Methods:30 SD male rats were randomly divided into three groups: the normal control (NC group), high fructose diet
(HFD group, feeding with 8%high fructose water), endotoxin group（LPS group, subcutaneous injection; 300 ug·kg-1·d-1）. At the end of
eight weeks after the glucose tolerance test, plasma endotoxin (LPS) and lipids were measured. Homeostasis model assessment-insulin resistance（
HOMA-IR）was calculated. The expression of pro-inflammatory factor ( tumor necrosis factor-alpha,TNF-slpha; interleukin-6, IL-6).
Observation of liver tissue pathological changes, the expression of insulin signal transduction proteins of insulin receptor substrate 1
(IRS-1) and P-IRS1Tyr632 and endotoxin receptor proteins TLR-4 in hepatic tissue were measured by western blot.Results:Compared
with NC group, the levels of rat plasma LPS, blood lipids（TG、TC、FFA、HDL）, pro-inflammatory factors（TNF-alpha, IL-6）, FPN, FINS and
HOMA-IR in the HFD group and LPS group are significantly increased and statistically significant（P＜0.05, P＜0.01）, whereas the ratio
of insulin receptor substrate P-IRS1/IRS1 and the level of endotoxin receptor proteins TLR-4 is increased（P＜0.05 P＜0.01）in the HFD
group and LPS group compared with NC group. HFD group and LPS group have no statistically significant differences in above-mentioned
parameters.Conclusion:Based on the experimental results, the present study demonstrates that high fructose diet and subcutaneous
injection of LPS may induce metabolic diseases in rats, such as NAFLD, accompanied at the same time by metabolic endotoxemia.
It is speculated that LPS can cause insulin resistance through inflammatory mechanisms, thus causing and promoting the development of
NAFLD and other metabolic disease. |
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