2,3,7,8-Tetrachlorodibenzo-p-dioxin increases reliance on fats as a fuel source independently of diet: evidence that diminished carbohydrate supply contributes to dioxin lethality.
2,3,7,8-Tetrachlorodibenzo-p-dioxin increases reliance on fats as a fuel source independently of diet: evidence that diminished carbohydrate supply contributes to dioxin lethality.
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2,3,7,8-四氯二苯并-对二恶英会增加对脂肪作为独立于饮食的燃料来源的依赖：证据表明碳水化合物供应减少会导致二恶英致死。
DOI：
10.1016/0006-291x(91)91558-t
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发表时间：
1991
影响因子：
3.1
通讯作者：
Rifkind,AB
中科院分区：
文献类型：
--
作者：
Lentnek,M;Griffith,OW;Rifkind,AB
环境毒素2，3，7，8-四氯二苯并-对-二恶英（TCDD）引起消耗综合征，其特征为食欲减退、体脂肪损失、中间代谢改变和死亡。使用传统的实验室动物还没有解决是否TCDD影响中间代谢独立于食欲减退。我们用鸡胚来回答这个问题，它不需要外源性食物来提供能量。我们的研究结果表明，TCDD治疗增加依赖脂肪作为燃料来源的食物摄入量的变化，因此可以影响独立的食欲减退中介代谢。使用氨基肉毒碱抑制脂肪酸氧化的实验结果表明，TCDD治疗损害碳水化合物的生产，而不是其利用率，前一种效果有助于TCDD致死。
The environmental toxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes a wasting syndrome marked by hypophagia, loss of body fat, changes in intermediary metabolism and death. Use of conventional laboratory animals has not resolved whether or not TCDD affects intermediary metabolism independently of hypophagia. We used the chick embryo, which does not require an exogenous food supply for energy, to answer this question. Our results show that TCDD treatment increases dependence on fats as a fuel source independently of changes in food intake and therefore can affect intermediary metabolism independently of hypophagia. Results of experiments using aminocarnitine to inhibit fatty acid oxidation suggest that TCDD treatment impairs carbohydrate production rather than its utilization and that the former effect contributes to TCDD lethality.