Singer L K, York D A, Bray G A
Pennington Biomedical Research Center, Baton Rouge, LA 70808-4124, USA.
Obes Res. 1997 Nov;5(6):587-94. doi: 10.1002/j.1550-8528.1997.tb00580.x.
The purpose of this experiment was to determine if Osborne-Mendel (OM) rats, which are susceptible to dietary-induced obesity, and S5B/PL (S5B) rats, which are resistant to dietary-induced obesity, differ in their feeding responses to mercaptoacetate (MA), which blocks fatty acid oxidation, or 2-deoxy-D-glucose (2DG), which blocks glucose utilization. 2DG (100 mg/kg or 200 mg/kg) increased food intake in both strains of rats on a high-fat diet (56% energy from fat). Mercaptoacetate (600 mumol/kg) increased food intake in OM but not S5B rats on a high-fat diet. When maintained on a low-fat diet (10% energy from fat), MA (400 mumol/kg or 600 mumol/kg) stimulated food intake in OM rats, whereas S5B rats increased food intake only after the highest dose of MA (600 mumol/kg). MA stimulated carbohydrate and protein intake in OM rats maintained on a macronutrient selection diet, whereas S5B rats maintained on this diet did not significantly increase intake of any macronutrient after MA. These results demonstrate that OM and S5B rats have a similar food intake response to 2DG but a dissimilar response to MA. The variable response to MA in these strains may be due to a difference in peripheral or central signaling systems related to fatty acid oxidation or a difference in metabolic environments between the strains, which in turn affects the feeding response to MA. These studies suggest that a difference in control of fatty acid oxidation may account for the difference in susceptibility to obesity when eating a high-fat diet.
本实验的目的是确定易受饮食诱导肥胖影响的奥斯本-孟德尔（OM）大鼠和对饮食诱导肥胖具有抗性的S5B/PL（S5B）大鼠，在对阻断脂肪酸氧化的巯基乙酸（MA）或阻断葡萄糖利用的2-脱氧-D-葡萄糖（2DG）的摄食反应上是否存在差异。2DG（100毫克/千克或200毫克/千克）使两种品系的高脂饮食（脂肪提供56%能量）大鼠的食物摄入量增加。巯基乙酸（600微摩尔/千克）使高脂饮食的OM大鼠而非S5B大鼠的食物摄入量增加。当维持低脂饮食（脂肪提供10%能量）时，MA（400微摩尔/千克或600微摩尔/千克）刺激OM大鼠的食物摄入，而S5B大鼠仅在最高剂量的MA（600微摩尔/千克）后才增加食物摄入。MA刺激了采用常量营养素选择饮食的OM大鼠的碳水化合物和蛋白质摄入，而采用这种饮食的S5B大鼠在给予MA后并未显著增加任何常量营养素的摄入。这些结果表明，OM大鼠和S5B大鼠对2DG的食物摄入反应相似，但对MA的反应不同。这些品系对MA的反应差异可能是由于与脂肪酸氧化相关的外周或中枢信号系统存在差异，或者是品系间代谢环境的差异，进而影响了对MA的摄食反应。这些研究表明，脂肪酸氧化控制的差异可能是导致高脂饮食时肥胖易感性差异的原因。
