Abstract
Treatment of male rats (300 to 325 g) with 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD, 15 or 50 μg/kg) caused dose-dependent reductions in body weight, feed and water intakes, and fecal output. Urine output, however, was not altered by TCDD. Fecal energy loss, as a percentage of daily feed energy intake (kcal/day), was similar in control and TCDD-treated rats as was the percentage of feed energy absorbed by the gastrointestinal tract, i.e., digestible energy. These findings dispel the long-standing proposal that a gross malabsorption syndrome is responsible for weight loss in TCDD-treated rats and place greater emphasis on hypophagia as the reason for weight loss. In support of a central role for hypophagia, it was found that control rats pair-fed to rats treated with a sublethal dose of TCDD (15 μg/kg) lost almost the same amount of weight. However, from 15 to 50 days post-treatment, the pair-fed animals consistently maintained their weight at a 10- to 15-g higher level than age-matched TCDD-treated rats. To determine why this weight difference occurs, the efficiency of feed utilization from Day 30 to 45 post-treatment in ad libitum fed control and TCDD-treated rats (15 μg/kg) that were maintaining different levels of body weight was compared. First, daily feed intakes of TCDD-treated and control rats were determined from Day 25 to 30 post-treatment. Second, weight of both groups were lowered by reducing feed intake in two successive 5-day periods to 50 and 10% of the respective ad libitum level. Third, on Days 40 to 45, both groups were refed their prereduction level of intake but reduced in proportion to the intervening loss in metabolic tissue mass. At each level of feed energy reduction, weight losses observed in the TCDD-treated and control rats were equivalent. Furthermone, although given only prerestriction amounts of feed that were indexed to their reduced metabolic body size (body wt kg 0.75), both TCDD-treated and control rats gained weight rapidly and at similar rates during the refeeding period. Thus, rats treated with a sublethal dose of TCDD displayed normal efficiency of feed utiization but did so at a subnormal level of weight. That is, just like control rats, TCDD-treated rats increased their efficiency of feed utiilzation (weight gain/feed intake) but only when their body weight was caused to fall below the lower weight maintenance level determined by the TCDD dose administered. This difference in weight level, below which control and TCDD-treated rats increase their efficiency of feed utilization, might explain why pair-fed control rats maintained a slightly higher level of body weight than TCDD-treated animals while ingesting the same amount of feed.
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