首页> 美国卫生研究院文献>Biochemical Journal >Refeeding meal-fed rats increases lipoprotein lipase activity and deposition of dietary 14Clipid in white adipose tissue and decreases oxidation to 14CO2. The role of undernutrition.
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Refeeding meal-fed rats increases lipoprotein lipase activity and deposition of dietary 14Clipid in white adipose tissue and decreases oxidation to 14CO2. The role of undernutrition.

机译:喂食膳食喂养的大鼠可增加脂蛋白脂肪酶活性和白色脂肪组织中膳食14C脂质的沉积并减少氧化为14CO2的速度。营养不良的作用。

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摘要

Meal-fed (3 h) rats had a decreased food intake, body weight and carcass fat compared with rats fed ad libitum. On refeeding a chow meal containing [1-14C]triolein, the production of 14CO2 was lower (45%) and the accumulation of carcass [14C]lipid higher (37%) in the meal-fed rats. There was higher lipoprotein lipase activity and greater accumulation of [14C]lipid in the epididymal and subcutaneous adipose-tissue depots of the meal-fed rats. In contrast, heparin-releasable lipoprotein lipase was not increased in perfused hearts of meal-fed rats on refeeding. Return of meal-fed rats to feeding ad libitum reversed these changes before the restoration of body weight or carcass fat. Evidence is presented that decreased dietary intake rather than meal pattern is an important determinant of the alterations in adipose lipid metabolism in the meal-fed rat in response to a meal.
机译:与随意喂养的大鼠相比,进餐(3 h)大鼠的食物摄入,体重和car体脂肪减少。在进食含[1-14C]三油精的粗粉时,用粗粉喂养的大鼠中14CO2的生成量较低(45%),car体[14C]脂质的积累较高(37%)。进餐大鼠的附睾和皮下脂肪组织贮库中脂蛋白脂肪酶的活性更高,[14C]脂质的积累更高。相反,餐后喂养的老鼠的心脏在再喂养时,肝素可释放的脂蛋白脂肪酶没有增加。在恢复体重或cas体脂肪之前,将以膳食喂养的大鼠随意喂食可以逆转这些变化。有证据表明,饮食摄入量的减少而不是膳食模式的下降是决定膳食对进食的大鼠中脂肪脂质代谢变化的重要决定因素。

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