机译:糖原缺陷的发生有助于无法抑制Zucker糖尿病肥胖大鼠对高血糖和高胰岛素血症的反应而产生的肝葡萄糖产生。
Department of Molecular Physiology and Biophysics, Vanderb University School of Medicine, Nashville, Tennessee;
Department of Molecular Physiology and Biophysics, Vanderb University School of Medicine, Nashville, Tennessee;
Department of Molecular Physiology and Biophysics, Vanderb University School of Medicine, Nashville, Tennessee;
Department of Molecular Physiology and Biophysics, Vanderb University School of Medicine, Nashville, Tennessee;
Pfizer Inc., Groto Connecticut;
Pfizer Inc., Groto Connecticut;
Department of Molecular Physiology and Biophysics, Vanderb University School of Medicine, Nashville, Tennessee;
机译:肝葡萄糖循环不参与Zucker糖尿病肥胖大鼠的高血糖发展
机译:葡萄糖毒性是导致Zucker糖尿病性脂肪大鼠内源性葡萄糖生成和肝葡萄糖激酶受损的原因。
机译:果糖1,6-双磷酸酶的抑制作用可减少zucker糖尿病肥胖大鼠的过多内源性葡萄糖生成并减轻高血糖症。
机译:代谢综合征的残疾预防:运动训练组合治疗和阿托伐他汀对Zucker脂肪大鼠血浆葡萄糖和脂肪细胞的影响
机译:饮食中锌或n-3脂肪酸对fa / fa和lean Zucker大鼠高胰岛素血症,高脂血症和胰腺功能的影响
机译:糖原缺陷的发生有助于无法抑制Zucker糖尿病肥胖大鼠对高血糖和高胰岛素血症的反应而产生的肝葡萄糖产生。
机译:有缺陷的糖血糖发生有助于抑制抑制肝脏糖尿病脂肪大鼠的高血糖和高胰岛素血症的肝葡萄糖产生