Absence of increased oxygen consumption in brown adipose tissue of rats exhibiting "cafeteria" diet-induced thermogenesis

Abstract

Young male Sprague–Dawley rats were induced to overeat (~45%) by provision of a "cafeteria" (CAF) diet of palatable human foods. Normophagic rats fed a commercial chow or a semisynthetic diet served as controls. The CAF rats exhibited (a) the reduced food efficiency and the propranolol-inhibitable elevation in resting metabolic rate (resting [Formula: see text]) that are indicative of a facultative diet-induced thermogenesis (DIT) by which excess energy gain is resisted, and (b) certain changes in brown adipose tissue (BAT) that are among those taken as evidence for BAT as the effector of DIT, e. g., increased protein content and increased mitochondrial binding of GDP. To assess directly and quantitatively the contribution by BAT to the elevation in [Formula: see text] (apparent DIT) of the CAF rats, BAT O₂ consumption was determined (Fick principle) from measurements of tissue blood flow (microsphere method) and the arteriovenous difference in blood O₂ across interscapular BAT (IBAT). To obtain the measurements, the animals were fitted under halothane anesthesia with vascular cannulas for intraventricular injection of microspheres and sampling of arterial blood and the venous effluent of IBAT. After recovery from anesthesia and rewarming to normal body temperature the animals were placed singly in a temperature-controlled metabolic chamber and the measurements, which also included determination of resting [Formula: see text], were made 1.5–2 h later at about 11:30 h. As determined from measurements made at 28 °C (thermoneutrality) mean values of resting [Formula: see text] for the cannulated rats were unchanged from those of intact (unoperated) CAF or control rats. At either 28 or 24 °C (housing temperature) the CAF rats, although exhibiting the elevation in resting [Formula: see text] attributed to DIT, were found to have levels of BAT O₂ consumption no greater than those in the control rats. Thus, direct measurement of the metabolic rate of BAT in vivo produced no evidence for BAT as the effector of the DIT of CAF rats.