机译:尽管内质网应激增加,但激活PPARa可以改善高果糖喂养小鼠的肝胰岛素抵抗和脂肪变性。
Molecular Pharmacology for Diabetes Group, Health Innovations Research Institute and School of Health Sciences, RMIT University, Melbourne, Victoria, Australia;
Molecular Pharmacology for Diabetes Group, Health Innovations Research Institute and School of Health Sciences, RMIT University, Melbourne, Victoria, Australia;
Molecular Pharmacology for Diabetes Group, Health Innovations Research Institute and School of Health Sciences, RMIT University, Melbourne, Victoria, Australia;
Molecular Pharmacology for Diabetes Group, Health Innovations Research Institute and School of Health Sciences, RMIT University, Melbourne, Victoria, Australia;
Molecular Pharmacology for Diabetes Group, Health Innovations Research Institute and School of Health Sciences, RMIT University, Melbourne, Victoria, Australia;
Biology of Lipid Metabolism Laboratory, Department of Physiology, Monash University, Melbourne, Victoria, Australia;
Molecular Pharmacology for Diabetes Group, Health Innovations Research Institute and School of Health Sciences, RMIT University, Melbourne, Victoria, Australia;
机译:内质网应激激活鞘氨醇激酶2改善小鼠肝脂肪变性和胰岛素抵抗
机译:羟基吡咯醇通过调节内质网胁迫来改善胰岛素抵抗力,并防止饮食诱导的肥胖小鼠中的肝脏脂肪变性
机译:过氧化物酶体增殖物激活受体-δ激动剂治疗可减轻慢性酒精诱导的肝胰岛素抵抗和内质网应激
机译:作为乙醇摄入的后果,仿肝内质网糖基化的仿素损伤
机译:内质网氧化还原变化在内质网应激和蛋白质折叠受损在肥胖相关胰岛素抵抗中的潜在作用
机译:尽管内质网应激增加但PPARα的活化可改善高果糖喂养小鼠的肝胰岛素抵抗和脂肪变性。
机译:尽管内质网胁迫增加,但PPAR的激活改善了高果糖喂养小鼠中的肝胰岛素抵抗和脂肪变性