Abstract

The principal objective of this study was to quantitate the anatomical and biochemical parameters associated with the depletion of body fat by the pesticide, chlordecone (CD, or Kepone). Groups of 5 male Sprague-Dawley rats (150-175 g) were fed a control diet or a diet containing 100 ppm CD for 5, 15, or 20 d. After the treatment period, animals were killed by exsanguination. Weight of the period epididymal fat pads was taken as the anatomical marker for the depletion of body fat. Blood levels of acetoacetate, 3-hydroxybutyrate, and nonesterified fatty acids (NEFA) were measured as biochemical as biochemical markers for lipolysis of body fat depots. Serum enzymes (SGPT, ICD) and serum triglycerides were measured to assess liver damage. A consistent and significant difference was observed in the weight of epididymal fat pads between the control and each of the treatment groups. The reduction in epididymal fat reached a maximum of 60% in the CD-fed animals after 20 d. Circulating ketone bodies were not different in any of the treated-animal groups, indicating that CD treatment does not result in metabolic ketosis. Serum triglycerides and NEFA levels were not significantly different in treatment groups versus in controls. Serum transaminases and isocitrate dehydrogenase were not elevated by exposure to CD. These findings indicate that metabolic ketosis is not induced by dietary exposure to CD. Utilization of lipids as energy substrates appears to be the primary underlying mechanism responsible for the loss of body fat observed in CD-treated rats. It appears that CD induces a depletion of body fat stores as a consequence of altered energy balance of the animal.

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