I Prostanoid Receptor-Mediated Inflammatory Pathway Promotes Hepatic Gluconeogenesis Through Activation of PKA and Inhibition of AKT
文献类型：期刊论文
| 作者 | Yan, Shuai; Zhang, Qianqian; Zhong, Xiaojing; Tang, Juan; Wang, Yuanyang; Yu, Junjie; Zhou, Yi; Zhang, Jian; Guo, Feifan（郭非凡） ; Liu, Yi（刘浥）
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| 刊名 | DIABETES
 |
| 出版日期 | 2014 |
| 卷号 | 63期号:9页码:2911-2933 |
| 通讯作者 | Yu, Y (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Key Lab Food Safety Res, Inst Nutr Sci,Grad Sch, Shanghai, Peoples R China. |
| 英文摘要 | Nonsteroidal anti-inflammatory drugs (NSAIDs), including acetylsalicylic acid (ASA), improve glucose metabolism in diabetic subjects, although the underlying mechanisms remain unclear. In this study, we observed dysregulated expression of cyclooxygenase-2, prostacyclin biosynthesis, and the I prostanoid receptor (IP) in the liver's response to diabetic stresses. High doses of ASA reduced hepatic prostaglandin generation and suppressed hepatic gluconeogenesis in mice during fasting, and the hypoglycemic effect of ASA could be restored by IP agonist treatment. IP deficiency inhibited starvation-induced hepatic gluconeogenesis, thus inhibiting the progression of diabetes, whereas hepatic overexpression of IP increased gluconeogenesis. IP deletion depressed cAMP-dependent CREB phosphorylation and elevated AKT phosphorylation by suppressing PI3K-/PKC--mediated TRB3 expression, which subsequently downregulated the gluconeogenic genes for glucose-6-phosphatase (G6Pase) and phosphoenol pyruvate carboxykinase 1 in hepatocytes. We therefore conclude that suppression of IP modulation of hepatic gluconeogenesis through the PKA/CREB and PI3K-/PKC-/TRB3/AKT pathways contributes to the effects of NSAIDs in diabetes. |
| 类目[WOS] | Endocrinology & Metabolism |
| 研究领域[WOS] | Endocrinology & Metabolism |
| 关键词[WOS] | TRANSCRIPTION FACTOR FOXO1 ; GLUCOSE-METABOLISM ; INSULIN SENSITIVITY ; BERAPROST SODIUM ; MICE LACKING ; CELLS ; LIVER ; PROSTACYCLIN ; PROTEIN ; RESISTANCE |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000341505300010 |
| 公开日期 | 2016-02-26 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/424]  |
| 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 中国科学院上海生命科学研究院营养科学研究所_磷脂代谢与心血管疾病研究组 |
| 推荐引用方式 GB/T 7714 | Yan, Shuai,Zhang, Qianqian,Zhong, Xiaojing,et al. I Prostanoid Receptor-Mediated Inflammatory Pathway Promotes Hepatic Gluconeogenesis Through Activation of PKA and Inhibition of AKT[J]. DIABETES,2014,63(9):2911-2933. |
| APA | Yan, Shuai.,Zhang, Qianqian.,Zhong, Xiaojing.,Tang, Juan.,Wang, Yuanyang.,...&Yu, Ying.(2014).I Prostanoid Receptor-Mediated Inflammatory Pathway Promotes Hepatic Gluconeogenesis Through Activation of PKA and Inhibition of AKT.DIABETES,63(9),2911-2933. |
| MLA | Yan, Shuai,et al."I Prostanoid Receptor-Mediated Inflammatory Pathway Promotes Hepatic Gluconeogenesis Through Activation of PKA and Inhibition of AKT".DIABETES 63.9(2014):2911-2933. |
入库方式： OAI收割
来源：上海营养与健康研究所
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