中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
PRLR Regulates Hepatic Insulin Sensitivity in Mice via STAT5

文献类型:期刊论文

作者Yu, Junjie; Xiao, Fei; Zhang, Qian; Liu, Bin; Guo, Yajie; Lv, Ziquan; Xia, Tingting; Chen, Shanghai(陈上海); Li, Kai; Du, Ying
刊名DIABETES
出版日期2013
卷号62期号:9页码:3103-3113
通讯作者Guo, FF (reprint author), Chinese Acad Sci, Grad Sch, Shanghai Inst Biol Sci, Key Lab Nutr & Metab,Inst Nutr Sci, Shanghai, Peoples R China.
英文摘要Insulin resistance is one of the major contributing factors in the development of metabolic diseases. The mechanisms responsible for insulin resistance, however, remain poorly understood. Although numerous functions of the prolactin receptor (PRLR) have been identified, a direct effect on insulin sensitivity has not been previously described. The aim of our current study is to investigate this possibility and elucidate underlying mechanisms. Here we show that insulin sensitivity is improved or impaired in mice injected with adenovirus that overexpress or knock down PRLR expression, respectively. Similar observations were obtained in in vitro studies. In addition, we discovered that the signal transducer and activator of transcription-5 pathway are required for regulating insulin sensitivity by PRLR. Moreover, we observed that PRLR expression is decreased or increased under insulin-resistant (db/db mice) or insulin-sensitive (leucine deprivation) conditions, respectively, and found that altering PRLR expression significantly reverses insulin sensitivity under both conditions. Finally, we found that PRLR expression levels are increased under leucine deprivation via a general control non-derepressible 2/mammalian target of rapamycin/ribosomal protein S6 kinase-1-dependent pathway. These results demonstrate a novel function for hepatic PRLR in the regulation of insulin sensitivity and provide important insights concerning the nutritional regulation of PRLR expression.
类目[WOS]Endocrinology & Metabolism
研究领域[WOS]Endocrinology & Metabolism
关键词[WOS]PROLACTIN RECEPTOR ISOFORMS ; AMINO-ACID ; GLUCOSE-HOMEOSTASIS ; LIPID-METABOLISM ; PROSTATE-GLAND ; C/EBP-BETA ; LIVER ; GROWTH ; KINASE ; RESISTANCE
收录类别SCI
语种英语
WOS记录号WOS:000323421000017
公开日期2016-02-26
版本出版稿
源URL[http://202.127.25.144/handle/331004/428]  
专题中国科学院上海生命科学研究院营养科学研究所_代谢的遗传与营养调控研究组
推荐引用方式
GB/T 7714
Yu, Junjie,Xiao, Fei,Zhang, Qian,et al. PRLR Regulates Hepatic Insulin Sensitivity in Mice via STAT5[J]. DIABETES,2013,62(9):3103-3113.
APA Yu, Junjie.,Xiao, Fei.,Zhang, Qian.,Liu, Bin.,Guo, Yajie.,...&Guo, Feifan.(2013).PRLR Regulates Hepatic Insulin Sensitivity in Mice via STAT5.DIABETES,62(9),3103-3113.
MLA Yu, Junjie,et al."PRLR Regulates Hepatic Insulin Sensitivity in Mice via STAT5".DIABETES 62.9(2013):3103-3113.

入库方式: OAI收割

来源:上海营养与健康研究所

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