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鲱鱼油对胆碱缺乏诱导的肝脏鸟氨酸脱羧酶活性及肝细胞胰岛素受体结合的影响。

The effect of menhaden oil on choline-deficiency-induced hepatic ornithine decarboxylase activity and hepatocyte insulin receptor binding.

作者信息

Betschart J M, Kasturi S, Shinozuka H, Virji M A

机构信息

University of Pittsburgh, Department of Physiology-Pharmacology, School of Dental Medicine, PA 15261.

出版信息

Carcinogenesis. 1990 Jun;11(6):889-93. doi: 10.1093/carcin/11.6.889.

Abstract

The effects of menhaden oil on the choline-deficient (CD) diet tumor promotion regimen-induced alterations in hepatocyte insulin receptors and the cellular ornithine decarboxylase (ODC) activity have been investigated in this study. Male Sprague-Dawley rats exposed to the tumor-promoting regimen of a CD diet for 10 days showed increases in hepatic ODC activity from 2.68 +/- 0.42 pmol 14CO2/mg protein/h in the animals fed basal control chow (C) to 13.54 +/- 2.38 (P less than 0.02) in the rats fed CD diet. These changes in ODC occur simultaneously with the alterations in hormone receptor binding as reported previously for insulin. Replacement of the lipid present in the control diet with 15% menhaden oil (CMO) had no significant effect on ODC activity (0.91 +/- 0.21), or on the number of insulin receptors (206,000 +/- 37,000) and the Kd (7.4 +/- 1.6). Sequential treatment with 10 days of CD diet and then 10 days of the C diet, resulted in a reversal in the elevated, CD-induced hepatic ODC activity to the control levels; however, substituting 15% menhaden oil for the fat present in the CD diet (CDMO) enhanced this enzymatic activity. In contrast, both sequential and CDMO treatments prevented the insulin receptor alterations induced by the CD diet. These data demonstrate that the CD diet-induced insulin receptor alterations occur concurrently with the induction of ODC activity. But insulin receptor changes and the increased ODC activity are affected differently by CDMO treatment, suggesting that their induction by the CD diet is through distinct mechanisms and only the receptor alterations correspond with the tumor-promoting action of CD diet regimen.

摘要

本研究调查了鲱鱼油对胆碱缺乏(CD)饮食肿瘤促进方案诱导的肝细胞胰岛素受体改变以及细胞鸟氨酸脱羧酶(ODC)活性的影响。暴露于CD饮食肿瘤促进方案10天的雄性Sprague-Dawley大鼠,其肝脏ODC活性从喂食基础对照饲料(C)的动物的2.68±0.42 pmol 14CO2/毫克蛋白质/小时增加到喂食CD饮食的大鼠的13.54±2.38(P<0.02)。如先前报道的胰岛素情况一样,ODC的这些变化与激素受体结合的改变同时发生。用15%的鲱鱼油(CMO)替代对照饮食中的脂质,对ODC活性(0.91±0.21)、胰岛素受体数量(206,000±37,000)和Kd(7.4±1.6)均无显著影响。先给予10天CD饮食,然后给予10天C饮食的序贯处理,导致CD诱导的肝脏ODC活性升高逆转至对照水平;然而,用15%的鲱鱼油替代CD饮食中的脂肪(CDMO)则增强了这种酶活性。相比之下,序贯处理和CDMO处理均能预防CD饮食诱导的胰岛素受体改变。这些数据表明,CD饮食诱导的胰岛素受体改变与ODC活性的诱导同时发生。但CDMO处理对胰岛素受体变化和ODC活性增加的影响不同,这表明CD饮食对它们的诱导是通过不同机制,且只有受体改变与CD饮食方案的肿瘤促进作用相关。

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