生长激素对培养的大鼠肝细胞中过氧化物酶体增殖物激活受体表达的抑制作用。

Suppressive effect of growth hormone on the expression of peroxisome proliferator-activated receptor in cultured rat hepatocytes.

作者信息

Yamada J, Sugiyama H, Watanabe T, Suga T

机构信息

Department of Clinical Biochemistry, Tokyo University of Pharmacy and Life Science, Japan.

出版信息

Res Commun Mol Pathol Pharmacol. 1995 Oct;90(1):173-6.

PMID:8581344

Abstract

The effect of growth (GH) and thyroid hormones (triiodothyronine, T3) on the expression of peroxisome proliferator-activated receptor (PPAR alpha) was examined using Northern blotting in primary cultures of rat hepatocytes. Exposure of the hepatocytes to GH at the concentrations of 5-500 ng/ml for 1 day decreased the steady state level of PPAR mRNA by 20-30% compared with the control. The decrease in the mRNA level reached about 50% after a 5-day exposure to 50 or 500 ng/ml GH. However, the PPAR mRNA level was increased by 30-50% in hepatocytes exposed to T3 at 30 or 300 nM. These findings suggest the suppression of PPAR expression as a possible mechanism for the GH-mediated suppression of the induction of peroxisomal beta-oxidation caused by peroxisome proliferators (PPs), whereas T3 may act in the other way to exert its suppressive effect on the PP induction of peroxisomal enzymes.

摘要

利用Northern印迹法，在大鼠原代肝细胞培养物中研究了生长激素（GH）和甲状腺激素（三碘甲状腺原氨酸，T3）对过氧化物酶体增殖物激活受体（PPARα）表达的影响。将肝细胞暴露于浓度为5 - 500 ng/ml的GH中1天，与对照组相比，PPAR mRNA的稳态水平降低了20 - 30%。在暴露于50或500 ng/ml GH 5天后，mRNA水平的降低达到约50%。然而，在暴露于30或300 nM T3的肝细胞中，PPAR mRNA水平增加了30 - 50%。这些发现表明，PPAR表达的抑制可能是GH介导的对过氧化物酶体增殖物（PPs）引起的过氧化物酶体β-氧化诱导抑制的一种机制，而T3可能以另一种方式发挥作用，对PP诱导的过氧化物酶体酶产生抑制作用。