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PAR2 promotes impaired glucose uptake and insulin resistance in NAFLD through GLUT2 and Akt interference
Hepatology ( IF 12.9 ) Pub Date : 2022-05-23 , DOI: 10.1002/hep.32589 Andrew M. Shearer 1, 2 , Yanling Wang 1 , Elizabeth K. Fletcher 1 , Rajashree Rana 1 , Emily S. Michael 1 , Nga Nguyen 1 , Manal F. Abdelmalek 3 , Lidija Covic 1, 2 , Athan Kuliopulos 1, 2
Hepatology ( IF 12.9 ) Pub Date : 2022-05-23 , DOI: 10.1002/hep.32589 Andrew M. Shearer 1, 2 , Yanling Wang 1 , Elizabeth K. Fletcher 1 , Rajashree Rana 1 , Emily S. Michael 1 , Nga Nguyen 1 , Manal F. Abdelmalek 3 , Lidija Covic 1, 2 , Athan Kuliopulos 1, 2
Affiliation
Insulin resistance and poor glycemic control are key drivers of the development of NAFLD and have recently been shown to be associated with fibrosis progression in NASH. However, the underlying mechanisms involving dysfunctional glucose metabolism and relationship with NAFLD/NASH progression remain poorly understood. We set out to determine whether protease-activated receptor 2 (PAR2), a sensor of extracellular inflammatory and coagulation proteases, links NAFLD and NASH with liver glucose metabolism.
中文翻译:
PAR2通过GLUT2和Akt干扰促进NAFLD中受损的葡萄糖摄取和胰岛素抵抗
胰岛素抵抗和血糖控制不佳是 NAFLD 发展的关键驱动因素,并且最近被证明与 NASH 的纤维化进展有关。然而,涉及功能失调的葡萄糖代谢和与 NAFLD/NASH 进展的关系的潜在机制仍然知之甚少。我们着手确定蛋白酶激活受体 2 (PAR2)(一种细胞外炎症和凝血蛋白酶的传感器)是否将 NAFLD 和 NASH 与肝脏葡萄糖代谢联系起来。
更新日期:2022-05-23
中文翻译:
PAR2通过GLUT2和Akt干扰促进NAFLD中受损的葡萄糖摄取和胰岛素抵抗
胰岛素抵抗和血糖控制不佳是 NAFLD 发展的关键驱动因素,并且最近被证明与 NASH 的纤维化进展有关。然而,涉及功能失调的葡萄糖代谢和与 NAFLD/NASH 进展的关系的潜在机制仍然知之甚少。我们着手确定蛋白酶激活受体 2 (PAR2)(一种细胞外炎症和凝血蛋白酶的传感器)是否将 NAFLD 和 NASH 与肝脏葡萄糖代谢联系起来。