Hyperuricemia contributes to glucose intolerance of hepatic inflammatory macrophages and impairs the insulin signaling pathway <i>via</i> IRS2-proteasome degradation.
第一作者:
Hairong,Zhao
第一单位:
Department of Endocrinology, Xiang'an Hospital of Xiamen University, Xiamen University, Xiamen, China.
作者:
主题词
AMP活化蛋白激酶类(AMP-Activated Protein Kinases);动物(Animals);细胞因子类(Cytokines);糖尿病, 2型(Diabetes Mellitus, Type 2);氟脱氧葡萄糖F18(Fluorodeoxyglucose F18);葡萄糖(Glucose);葡糖耐受不良(Glucose Intolerance);葡萄糖转运体4型(Glucose Transporter Type 4);高尿酸血症(Hyperuricemia);胰岛素(Insulin);胰岛素受体底物蛋白质类(Insulin Receptor Substrate Proteins);胰岛素抗药性(Insulin Resistance);枯否细胞(Kupffer Cells);小鼠(Mice);磷酸肌醇3-激酶类(Phosphatidylinositol 3-Kinases);蛋白酶体内肽酶复合物(Proteasome Endopeptidase Complex);原癌基因蛋白质c-akt(Proto-Oncogene Proteins c-akt);信号传导(Signal Transduction);TOR丝氨酸-苏氨酸激酶(TOR Serine-Threonine Kinases);尿酸氧化酶(Urate Oxidase);尿酸(Uric Acid)
DOI
10.3389/fimmu.2022.931087
PMID
36177037
发布时间
2022-10-03
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Frontiers in immunology
931087页
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