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机译:ImidaCloprid在雌性C57BL / 6J小鼠中促进高脂肪饮食诱导的肥脂,并通过AMPKα介导的途径增强3T3-L1脂肪细胞的脂肪组织
Department of Food Science Department of Mathematics and Statistics and Department of Veterinary and Animal Sciences University of Massachusetts Amherst Massachusetts 01003 United States;
Department of Food Science Department of Mathematics and Statistics and Department of Veterinary and Animal Sciences University of Massachusetts Amherst Massachusetts 01003 United States;
Department of Food Science Department of Mathematics and Statistics and Department of Veterinary and Animal Sciences University of Massachusetts Amherst Massachusetts 01003 United States;
Department of Food Science Department of Mathematics and Statistics and Department of Veterinary and Animal Sciences University of Massachusetts Amherst Massachusetts 01003 United States;
Department of Food Science Department of Mathematics and Statistics and Department of Veterinary and Animal Sciences University of Massachusetts Amherst Massachusetts 01003 United States;
Department of Biological Sciences and Environmental Sciences Program Southern Illinois University Edwardsville Illinois 62026 United States;
Department of Food Science Department of Mathematics and Statistics and Department of Veterinary and Animal Sciences University of Massachusetts Amherst Massachusetts 01003 United States;
Department of Food Science Department of Mathematics and Statistics and Department of Veterinary and Animal Sciences University of Massachusetts Amherst Massachusetts 01003 United States;
adiposity; AKT; AMPKα; imidacloprid; insulin resistance; neonicotinoids;
机译:ImidaCloprid在雌性C57BL / 6J小鼠中促进高脂肪饮食诱导的肥脂,并通过AMPKα介导的途径增强3T3-L1脂肪细胞的脂肪组织
机译:5,7-二甲氧基黄酮通过抑制3T3-L1脂肪细胞和高脂饮食诱导的肥胖C57BL / 6J小鼠的脂肪生成来减轻肥胖。
机译:通过抑制3T3-L1脂肪细胞和高脂肪饮食诱导的肥胖C57BL / 6J小鼠的脂肪发生,5,7-二甲氧基氟氟酮通过抑制脂肪发生而衰减肥胖症
机译:苯并噻唑衍生物在长期高脂肪喂养C57BL / 6J小鼠中加速了总甾醇的排泄
机译:长期饮食锌处理对饮食性肥胖C57BL / 6J小鼠糖尿病指数和脂肪组织磷脂和甘油三酸酯脂肪酸组成的影响
机译:吡虫啉促进高脂饮食诱导的肥胖雌性C57BL / 6J小鼠体内的表达并增强3T3-L1脂肪细胞中的脂肪形成通过AMPKα介导的途径
机译:黄粉虫幼虫通过ampK和mapKs抑制脂肪生成3T3-L1脂肪细胞中的信号传导和高脂饮食诱导的肥胖小鼠的肥胖