Moustaïd N, Hainque B, Quignard-Boulange A, Pairault J
INSERM U177 15, Paris, France.
Reprod Nutr Dev. 1990;30(3):317-24.
Preadipocyte subclones derived from mouse 3T3 cells differentiate into adipocytes; this differentiation is characterized by an increased activity of numerous enzymes required for triglyceride synthesis and/or mobilization. Among these enzymes, the role of glycerophosphate dehydrogenase in the differentiation process has been previously reported. In the present work, we studied the hormonal regulation of glycerophosphate dehydrogenase gene expression (G3PDH) in differentiated 3T3-F442A adipocytes. Dexamethasone (DEX) elicited a 50% decrease in both mRNA content and specific activity of G3PDH. This effect was due to a posttranscriptional event since DEX shortened the half life of the mRNA, whereas it did not modify the transcription rate of this gene. The DEX effect is specific to G3PDH, since the expression of another adipose-specific gene, namely adipsin, is not modified by DEX treatment. Insulin counteracts the inhibitory effect of DEX, mainly by stabilizing the mRNA encoding for G3PDH. The antiglucocorticoid RU38486 is able to reverse DEX inhibition. Latter phenomenon suggests that DEX action on G3PDH gene expression could be mediated by glucocorticoid receptors.
从小鼠3T3细胞衍生而来的前脂肪细胞亚克隆可分化为脂肪细胞;这种分化的特征是甘油三酯合成和/或动员所需的多种酶的活性增加。在这些酶中,磷酸甘油脱氢酶在分化过程中的作用此前已有报道。在本研究中,我们研究了分化的3T3-F442A脂肪细胞中磷酸甘油脱氢酶基因表达(G3PDH)的激素调节。地塞米松(DEX)使G3PDH的mRNA含量和比活性均降低50%。这种效应是由于转录后事件引起的,因为DEX缩短了mRNA的半衰期,而没有改变该基因的转录速率。DEX对G3PDH的作用具有特异性,因为另一个脂肪特异性基因即脂肪酶的表达不受DEX处理的影响。胰岛素主要通过稳定编码G3PDH的mRNA来抵消DEX的抑制作用。抗糖皮质激素RU38486能够逆转DEX的抑制作用。后一种现象表明,DEX对G3PDH基因表达的作用可能是由糖皮质激素受体介导的。