Effect of nafenopin, a peroxisome proliferator, on energy metabolism in the rat as a function of acclimation temperature.

The effects of the peroxisome proliferator, nafenopin, on body temperature, apparent gross food efficiency and activity of interscapular brown adipose tissue (IBAT) peroxisomes and mitochondria of rats acclimated at 23 degrees C or at 32 degrees C have been studied. In 23 degrees C-acclimated rats, nafenopin treatment induced an atrophy of IBAT characterized by a decrease of tissue wet weight, of amounts of mitochondrial and peroxisomal proteins and of mitochondrial total succinate dehydrogenase activity to 67%, 67%, 65% and 57%, respectively of control values. It also resulted in a 1.9-fold stimulation of peroxisome total acyl CoA oxidase activity and had no effect on apparent gross food efficiency or colonic temperature. Acclimation at 32 degrees C per se induced an atrophy of IBAT and a decrease of total catalase and acyl CoA oxidase activities to 23% and 35%, respectively of values obtained in rats acclimated at 23 degrees C. Nafenopin treatment had no effect on IBAT wet weight, on the amounts of mitochondrial and peroxisomal proteins or on total succinate dehydrogenase activity; it resulted in a 2.9- and a 3.7-fold stimulation of the catalase and acyl CoA oxidase activities, respectively with no change in IBAT oxygen consumption. Apparent gross food efficiency was decreased to 54% of control value and colonic temperature increased by 0.91 degrees C. These results may be interpreted in the following way: nafenopin may, at 23 degrees C ambient temperature, induce an extra-heat production in other tissues than IBAT. This extra-heat production is fully compensated via the thermoregulatory feedback control. This compensation cannot occur at thermoneutrality.