2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN-INDUCED ANOREXIA AND WASTING SYNDROME IN RATS - AGGRAVATION AFTER VENTROMEDIAL HYPOTHALAMIC-LESION

Long-term regulation of body weight and food intake were studied after rats were subjected to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), wh ich causes hypophagia and body weight loss, and to ventromedial hypoth alamic lesion, which causes hyperphagia, metabolic changes and obesity . These two factors appeared to have an interaction, as ventromedial h ypothalamic lesion initially aggravated the effects of TCDD on body we ight and food intake. This was seen in both TCDD-resistant and TCDD-su sceptible rat strains. In contrast, if TCDD was given several weeks be fore the lesion and body weight had stabilized to a low level, no aggr avation was seen, bur TCDD completely blocked the effects of ventromed ial hypothalamic lesion. Thus, TCDD seems to affect the same regulatio n chain that is involved in the lesioning of the ventromedial hypothal amus. TCDD might serve as a tool in studying different mechanisms of l ong-term food intake and body weight regulation.