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胰岛素抵抗在降低荷瘤大鼠脂蛋白脂肪酶活性中的作用。

Role of insulin resistance in decreasing lipoprotein lipase activity in tumor-bearing rats.

作者信息

Noguchi Y, Nomura K, Yoshikawa T, Fukuzawa K, Makino T, Tsuburaya A, Matsumoto A

机构信息

First Department of Surgery, Yokohama City University School of Medicine, Japan.

出版信息

Surg Today. 1996;26(4):271-5. doi: 10.1007/BF00311587.

Abstract

The role of insulin resistance in the tumor-induced decrease in tissue lipoprotein lipase (LPL) activity was studied in vivo and vitro in methylcholanthrene-induced sarcoma-bearing rats. Intraperitoneal (i.p.) injection of 2U of regular insulin resulted in high-adipose LPL activity in control rats (CTR) of 122.0 +/- 42.4 U/mg tissue, but it had little effect on tumor-bearing rats (TBR), which showed a value of only 9.6 +/- 5.5 U/mg tissue (P = 0.002). When adjusted for serum insulin concentrations, adipose LPL activity remained significantly different between the TBR and CTR at 0.19 +/- 0.17 and 0.78 +/- 0.29 U/mg tissue, respectively (P = 0.02). Following the in vitro incubation with either 1.44 g/l glucose of 1 x 10-8 U insulin of adipose tissue fragments obtained from the TBR and the CTR, measurable LPL activity was maintained in the tissue from the CTR for 2 h but not in that from the TBR. These results suggest that the decreased LPL activities seen in the tumor-bearing state may be mediated by insulin resistance.

摘要

在体内和体外研究了胰岛素抵抗在甲基胆蒽诱导的荷肉瘤大鼠肿瘤诱导的组织脂蛋白脂肪酶(LPL)活性降低中的作用。腹腔注射2U普通胰岛素后,对照大鼠(CTR)的高脂肪LPL活性为122.0±42.4U/mg组织,但对荷瘤大鼠(TBR)几乎没有影响,后者的值仅为9.6±5.5U/mg组织(P = 0.002)。根据血清胰岛素浓度进行调整后,TBR和CTR之间的脂肪LPL活性仍存在显著差异,分别为0.19±0.17和0.78±0.29U/mg组织(P = 0.02)。用从TBR和CTR获得的脂肪组织片段与1.44g/l葡萄糖或1×10-8U胰岛素进行体外孵育后,CTR组织中的LPL活性可维持2小时,而TBR组织中的LPL活性则不能维持。这些结果表明,荷瘤状态下LPL活性降低可能由胰岛素抵抗介导。

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