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作 者:张斌[1] 张利华[1] 李宁[1] 汪义军[1] 黎介寿[1]
机构地区:[1]南京军区南京总医院普通外科研究所
出 处:《世界华人消化杂志》1999年第4期335-337,共3页World Chinese Journal of Digestology
摘 要:目的研究n3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05mg.术后3d测定各组大鼠血清TNF,IL6,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RTPCR的方法,检测TNFmRNA的表达.结果FO组大鼠CLP3d后血清TNF,IL6,PGE2,基础血糖,胰岛素水平明显低于CLP对照组(P<005),而KI值及肌肉中葡萄糖含量显著增高(P<005).注射TNF抗体尽管能降低血清TNF浓度,但对IL6,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>005).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.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.
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