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.

Abstract:

: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.

authors

Lentnek M,Griffith OW,Rifkind AB

doi

10.1016/0006-291x(91)91558-t

subject

Has Abstract

pub_date

1991-02-14 00:00:00

pages

1267-71

issue

3

eissn

0006-291X

issn

1090-2104

pii

0006-291X(91)91558-T

journal_volume

174

pub_type

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