Prolactin regulatory element-binding protein is involved in suppression of the adiponectin gene in vivo
Prolactin regulatory element-binding protein is involved in suppression of the adiponectin gene in vivo
复制标题
催乳素调节元件结合蛋白参与体内脂联素基因的抑制
DOI：
10.1007/s40618-016-0589-3
复制
发表时间：
2017
影响因子：
5.4
通讯作者：
Murao K
中科院分区：
文献类型：
--
作者：
Zhang XZ;Imachi H;Lyu JY;Fukunaga K;Sato S;Ibata T;Kobayashi T;Yoshimoto T;Kikuchi F;Dong T;Murao K
催乳素调节元件结合蛋白（PreB）是WD重复序列蛋白家族的成员之一，是调节大鼠垂体前叶催乳素启动子活性的转录因子。PREB不仅在垂体中表达，而且在包括脂肪组织在内的各种其它组织中表达。先前的研究表明，PREB作为一种转录调节因子，抑制脂联素基因在培养的3 T3 L1前脂肪细胞中的表达。本研究的目的是进一步研究PREB在体内脂肪组织中的潜在作用。方法产生过表达PREB的转基因小鼠（PREB转基因小鼠）。使用葡萄糖和胰岛素耐量试验评价PREB转基因小鼠的胰岛素抵抗。通过蛋白质印迹分析和定量聚合酶链反应（qPCR）检测脂肪组织中脂联素的表达。硬脂酰辅酶A去饱和酶（Scd）和脂联素受体2（ADIPOR 2）的表达水平进行定量qPCR.ResultsGlucose和胰岛素耐量试验显示在PREB转基因小鼠的胰岛素抵抗。血清脂联素和瘦素浓度降低。脂肪组织中脂联素基因表达降低，这通过PREB转基因小鼠肝脏中脂联素依赖性肝Scd基因的下调和ADIPOR 2基因的上调得到证实。我们还发现，吡格列酮，过氧化物酶体增殖物激活受体-R的激动剂，改善胰岛素抵抗的PREB转基因小鼠后，10天的喂养periods.ConclusionsThese结果表明，PREB可能有助于调节脂联素基因的表达在体内。
PurposeProlactin regulatory element-binding protein (PREB), a member of the WD-repeat protein family, has been recognized as a transcriptional factor that regulates prolactin promoter activity in the anterior pituitary of rats. PREB is expressed not only in the pituitary but also in various other tissues, including the adipose tissue. Previous studies have shown that PREB acts as a transcriptional regulator and suppresses the expression of the adiponectin gene in cultured 3T3L1 preadipocytes. The aim of this study was to further examine the potential role of PREB in adipose tissue in vivo.MethodsTransgenic mice that overexpressing PREB (PREB transgenic mice) were generated. Insulin resistance was evaluated in PREB transgenic mice using glucose and insulin tolerance tests. Adiponectin expression in the adipose tissue was examined by western blot analysis and quantitative polymerase chain reaction (qPCR). The expression levels of stearoyl-CoA desaturase (Scd) and adiponectin receptor 2(ADIPOR2) were quantified by qPCR.ResultsGlucose and insulin tolerance tests revealed insulin resistance in PREB transgenic mice. Serum adiponectin and leptin concentrations were decreased. Adiponectin gene expression was decreased in the adipose tissue, which was confirmed by the downregulation of the adiponectin-dependent hepatic Scd gene and upregulation of the ADIPOR2 gene in the liver of PREB transgenic mice. We also found that pioglitazone, an agonist for the peroxisome proliferator-activated receptor-r, improved the insulin resistance in the PREB transgenic mice after a 10-day feeding period.ConclusionsThese results demonstrated that PREB might contribute to the regulation of adiponectin gene expression in vivo.