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目的观察高脂饮食饲养造成的肝脏胰岛素抵抗与肝糖输出有关的调控基因表达的关系。方法将8周龄雄性SD大鼠随机分为2组:正常饲养组(10例)和高脂饮食饲养组(10例)。饲养期间动态观察体重和空腹血糖变化趋势。饲养至28周实验终点时取空腹血测胰岛素和甘油三酯。采用肝脏对3H-2- 脱氧葡萄糖的摄取能力测定各组的肝脏胰岛素敏感性,用蒽酮法测定肝糖原含量,并用逆转录聚合酶链反应法分析糖异生和糖原合成关键酶肝脏磷酸烯丙醇羧激酶、葡萄糖-6-磷酸酶、糖原合成酶和PPAR γ协同刺激因子1 α的mRNA表达的变化。结果高脂饮食饲养大鼠出现明显腹型肥胖。血浆甘油三酯水平升高。饲养18周开始,高脂饮食组空腹血糖增加[正常饲养组(4．77±0．63)mmol／L,高脂饮食组[(5．45± 0.87)mmol／L,P<0．05],此差异持续到28周;肝脏3H-2-脱氧葡萄糖摄取率高脂饮食组较正常饲养组下降42．0％,肝糖原含量增加92．4％(P<0．01)l磷酸烯丙醇羧激酶mRNA增加41．5％,协同刺激因子1α mRNA增加30．8％(P<0．05)。结论长期高脂饮食诱导肝脏协同刺激因子1α和肝脏磷酸烯丙醇羧激酶基因表达,糖异生增加,同时肝糖分解不能相应受到抑制,导致肝糖输出增加及空腹血糖升高。
Objective To observe the relationship between hepatic insulin resistance and regulation of hepatic glucose export-related gene expression induced by high-fat diet. Methods 8-week-old male Sprague-Dawley rats were randomly divided into two groups: normal group (10 cases) and high-fat diet group (10 cases). Dynamic observation of body weight and fasting blood glucose during feeding trends. Feeding to 28 weeks of the end of the experiment when taking fasting blood test insulin and triglycerides. The hepatic insulin sensitivity of each group was determined by liver uptake of 3H-2-deoxyglucose, liver glycogen content was determined by anthrone method, and gluconeogenesis and glycogen synthesis key enzyme liver were analyzed by reverse transcription polymerase chain reaction Allyl alcohol carboxykinase, glucose-6-phosphatase, glycogen synthase and PPAR gamma co-stimulatory factor 1 alpha mRNA expression changes. Results The rats fed high-fat diet showed significant abdominal obesity. Plasma triglyceride levels are elevated. From 18 weeks of feeding, fasting blood glucose increased in the high-fat diet group (4.77 ± 0.63 mmol / L in the normal diet group [(5.45 ± 0.87) mmol / L, P <0.05 ], The difference lasted for 28 weeks; liver 3H-2-deoxyglucose uptake rate of high-fat diet group decreased 42.0%, liver glycogen content increased 92.4% (P <0.01) Allyl alcohol carboxykinase mRNA increased by 41.5% and co-stimulatory factor 1α mRNA increased by 30.8% (P <0.05). Conclusion Long-term high-fat diet induces gene expression of hepatic co-stimulatory factor 1α and liver phospholipid alcohol kinase, and gluconeogenesis increases. At the same time, glycogen breakdown can not be inhibited correspondingly, resulting in increased hepatic glucose output and elevated fasting plasma glucose.