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.
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.
Lentnek
M
M
Department of Pharmacology, Cornell University Medical College, New York, N.Y. 10021.
Griffith
O W
OW
Rifkind
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D000818:Animals; D001622:Betaine / Q000031:analogs & derivatives* / Q000494:pharmacology; D002331:Carnitine; D002642:Chick Embryo; D004041:Dietary Fats; D004146:Dioxanes / Q000494:pharmacology; D007700:Kinetics; D010101:Oxygen Consumption / Q000187:drug effects*; D000072317:Polychlorinated Dibenzodioxins / Q000494:pharmacology*
D004041:Dietary Fats; D004146:Dioxanes; D000072317:Polychlorinated Dibenzodioxins; D001622:Betaine; C045761:emeriamine; C025223:1,4-dioxane; D002331:Carnitine