n-3脂肪酸对感染大鼠糖代谢异常的调控作用及其机制

目的研究ｎ３脂肪酸对ＣＬＰ大鼠糖代谢的影响，并探讨其调控作用的可能机制．方法♂ＳＤ大鼠３０只，分为ＣＬＰ、抗ＴＮＦ及ＦＯ三组，ｎ＝１０．ＦＯ组每天以鱼油１ｍＬ，ｉｇ３ｗｋ后皆作ＣＬＰ手术，抗ＴＮＦ组于术前术后腹腔内注射ＴＮＦ抗体０５ｍｇ．术后３ｄ测定各组大鼠血清ＴＮＦ，ＩＬ６，胰岛素，糖皮质激素及ＰＧＥ２水平，并作胰岛素耐量试验观察胰岛素敏感指数ＫＩ的变化．同时，活检后腿肌肉，测定葡萄糖的含量，并用ＲＴＰＣＲ的方法，检测ＴＮＦｍＲＮＡ的表达．结果ＦＯ组大鼠ＣＬＰ３ｄ后血清ＴＮＦ，ＩＬ６，ＰＧＥ２，基础血糖，胰岛素水平明显低于ＣＬＰ对照组（Ｐ＜００５），而ＫＩ值及肌肉中葡萄糖含量显著增高（Ｐ＜００５）．注射ＴＮＦ抗体尽管能降低血清ＴＮＦ浓度，但对ＩＬ６，ＰＧＥ２血糖，胰岛素浓度及ＫＩ值，骨骼肌葡萄糖含量却无明显影响（Ｐ＞００５）．喂食３ｗｋ鱼油能降低周围肌肉中ＴＮＦ的表达（约６０％），而间断注射ＴＮＦ抗体则无明显改变．结论鱼油不仅能降低感染机体的应激反应，改善糖代谢，而且能通过下调周围肌肉中ＴＮＦ的表达，缓解由其诱导的胰岛素抵抗．

Effects of n 3 fatty acids on glucose metabolism of septic rats and its mechanism

AIM To study the effects of n 3 fatty acids on glucose metabolism of CLP rats, and the possible mechanism of its modulation action. METHODS Thirty male SD rats were assigned into three groups: CLP, anti-TNF and FO. Rats in FO group were fed with 1 mL fish oil daily through gastric gavage. After 3 weeks, all rats in three groups underwent CLP operation, while the rats in anti TNF group were injected with TNF monoclonal antibody 0 5 mg ip before and after operation. On the third day serum levels of TNF, IL 6, insulin, glucoscocoid and PGE 2 were assessed and insulin tolerance test was accomplished to calculate insulin sensitivity index (KI). Skeletal muscle biopsy was used to detect the content of glucose and expression of TNF. RESULTS Serum levels of TNF, IL 6, PGE 2, basal glucose and insulin were significantly lower in rats of FO group than those of CLP group ( P <0 05), but KI and content of glucose in muscle were much higher ( P <0 05). Although injection of TNF antibody can lower blood TNF concentration, it showed no effect on levels of IL 6, PGE 2 glucose, insulin KI and content of muscle glucose ( P >0 05). Fish oil feeding can dramatically decrease TNF expression in peripheral muscle compared with injection of TNF antibody. CONCLUSION Fish oil can not only attenuate the stress response of septic host, improve glucose metabolism, but also can down regulate TNF expression in peripheral tissues, thus alleviating insulin resistance induced by its overexpression.