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 Academic Article Article uri icon

Overview

MeSH Major

  • Antidepressive Agents
  • Anxiety Disorders
  • Cycloserine
  • Excitatory Amino Acid Agonists
  • Implosive Therapy
  • N-Methylaspartate
  • Obsessive-Compulsive Disorder
  • Outcome Assessment (Health Care)
  • Stress Disorders, Post-Traumatic

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.

publication date

  • February 14, 1991

Research

keywords

  • Academic Article

Identity

Digital Object Identifier (DOI)

  • 10.1016/0006-291X(91)91558-T

PubMed ID

  • 1996990

Additional Document Info

start page

  • 1267

end page

  • 71

volume

  • 174

number

  • 3