Arch J R
Am J Clin Nutr. 1981 Dec;34(12):2763-9. doi: 10.1093/ajcn/34.12.2763.
The study investigated whether changes in body composition of normal and genetically obese C57BL/6J (ob/ob) mice caused by the anorectic drugs phentermine, diethylpropion, fenfluramine, and mazindol are entirely due to reduced food intake. Mice were dosed daily (25 mg/kg po) for 28 days after which time carcass composition was determined. Compared to controls fed at libitum, reductions in food intake were for phentermine, 7%; fenfluramine, 17%; diethylpropion, 17%, whereas reduction in body lipid content were for phentermine, 16%; mazindol, 18%; fenfluramine, 8%; diethylpropion, 10%. Since diet restriction by 22% (in the absence of treatment with any drug) resulted in a body lipid content 12% below that of controls fed ad libitum, these results suggest that some of the lipid loss caused by phentermine and possibly mazindol is due to increased energy expenditure. In support of this conclusion, phentermine and mazindol increased energy expenditure in normal mice by 35% compared to untreated controls in the 6 h after dosing but diethylpropion and fenfluramine had little or no effect. Determination of the carcass composition of the normal mice confirmed that phentermine has a metabolic antiobesity effect. Fenfluramine had an unexpected effect on carcass composition in normal mice.
该研究调查了食欲抑制药物芬特明、二乙胺苯丙酮、芬氟拉明和马吲哚导致正常及遗传性肥胖的C57BL/6J（ob/ob）小鼠身体成分变化是否完全归因于食物摄入量减少。小鼠每天口服给药（25毫克/千克），持续28天，之后测定尸体成分。与自由进食的对照组相比，芬特明的食物摄入量减少了7%；芬氟拉明减少了17%；二乙胺苯丙酮减少了17%，而身体脂质含量的减少量分别为：芬特明16%；马吲哚18%；芬氟拉明8%；二乙胺苯丙酮10%。由于在不使用任何药物治疗的情况下，将饮食限制22%会导致身体脂质含量比自由进食的对照组低12%，这些结果表明，芬特明以及可能的马吲哚所导致的部分脂质损失是由于能量消耗增加所致。支持这一结论的是，与给药后6小时未治疗的对照组相比，芬特明和马吲哚使正常小鼠的能量消耗增加了35%，但二乙胺苯丙酮和芬氟拉明几乎没有影响或没有影响。对正常小鼠尸体成分的测定证实，芬特明具有代谢性抗肥胖作用。芬氟拉明对正常小鼠的尸体成分有出人意料的影响。
