The net in vivo uptake or release of free fatty acids glycerol, glucose, lactate, and pyruvate by the interscapular brown adipose tissue (IBAT) of barbital-anesthetized, cold-acclimated rats was determined from measurements of plasma arteriovenous concentration differences across IBAT and tissue blood flow. Measurements were made without stimulation of the tissue and also during submaximal and maximal stimulation by infused noradrenaline (NA), the physiological activator of BAT thermogenesis. There was no appreciable uptake of glucose or release of fatty acids and glycerol by the nonstimulated tissue. At both levels of stimulation there was significant uptake of glucose (1.7 and 2.0 mumol/min) and release of glycerol (0.9 and 1.2 mumol/min), but only at maximal stimulation was there significant release of fatty acids (1.9 mumol/min). Release of lactate and pyruvate accounted for 33% of the glucose taken up at submaximal stimulation and 88% at maximal stimulation. By calculation, the remainder of the glucose taken up was sufficient to have fueled about 12% of the thermogenesis at submaximal stimulation, but only about 2% at maximal stimulation. As estimated from the rate of glycerol release, the rate of triglyceride hydrolysis was sufficient at submaximal stimulation to fuel IBAT thermogenesis entirely with the resulting fatty acids, but it was not sufficient to do so at maximal stimulation when some of the fatty acid was exported. It is suggested that at maximal NA-induced thermogenesis a portion of lipolysis proceeded only to the level of mono- and di-glycerides with the result that glycerol release did not fully reflect the rate of fatty acid formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Starvation results in an energy-conserving reduction in metabolic rate that has features of an adaptive response. Tissue and organ sites of this response were investigated by examining the effects of starvation for 5 d on tissue blood flow (microsphere method) and regional arteriovenous O2 differences ((a-v)O2) in conscious rats resting quietly at 28 degrees C. Comparison was with fed and overnight-fasted animals. Whole body resting metabolic rates (MR), colonic temperatures (Tc), and tissue weights were also determined. Quantitative changes in energy expenditure (as O2 consumption) were obtained for two regions: the portal-drained viscera (PDV) and the hindquarters (HQ). Fasting overnight resulted in increased blood flow to white adipose tissue (WAT) and decreased flow to the brain, PDV, testes, and skin; however, MR, Tc, the two regional ((a-v)O2, and the weights of most tissues were not significantly altered. In comparison with overnight fasting, starvation for 5 d resulted in a 13% reduction in body weight, weight loss in many tissues and organs, a 26% reduction in MR, a decline of 0.5 degree C in Tc, decreased (a-v)O2 across both the PDV and HQ, reduced cardiac output, and decreased blood flow to the heart, PDV, skin, WAT, leg muscle, HQ, and the musculoskeletal body as a whole. Utilization of O2 by the PDV and HQ (flow X (a-v)O2) declined by amounts that accounted for 22 and 18%, respectively, of the reduction in MR. The reductions in cardiac output (18%) and heart blood flow (36%) indicate that the heart also made a contribution to energy conservation (roughly estimated as 5%).(ABSTRACT TRUNCATED AT 250 WORDS)

Young male Sprague-Dawley rats were induced to overeat (approximately 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 VO2) 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 VO2 (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 VO2, were made 1.5-2 h later about 11:30 h. As determined from measurements made at 28 degrees C (thermoneutrality) mean values of resting VO2 for the cannulated rats were unchanged from those of intact (unoperated) CAF or control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Diet-induced thermogenesis (DIT) in young rats overeating a "cafeteria" (CAF) diet of palatable human foods is characterized by a chronic, propranolol-inhibitable elevation in resting metabolic rate (VO2) and is associated with various changes in brown adipose tissue (BAT) that have been taken as evidence for BAT as the effector of DIT. But direct evidence for participation of BAT in DIT has been lacking. By employing a nonocclusive cannula to sample the venous effluent of interscapular BAT (IBAT) for analysis of its O2 content and measuring tissue blood flow with microspheres, we accomplished direct determination (Fick principle) of the O2 consumption of BAT in conscious CAF rats. In comparison with normophagic controls fed chow, the CAF rats exhibited a 43% increase in metabolizable energy intake, reduced food efficiency, a 22% elevation in resting VO2 at 28 degrees C (thermoneutrality) or 24 degrees C (housing temperature), and characteristic changes in the properties of their BAT (e.g., increased mass, protein content and mitochondrial GDP binding). They also exhibited the greater metabolic response to exogenous noradrenaline characteristic of CAF rats and the near elimination by propranolol of their elevation in VO2. By the criterion of their elevated VO2, the CAF rats were exhibiting DIT at the time of the measurements of BAT blood flow and blood O2 levels. However, BAT O2 consumption was found to be no greater in the CAF rats than in the controls at either 28 or 24 degrees C. At 28 degrees C it accounted for less than 1% of whole body VO2; at 24 degrees C it increased to about 10% of overall VO2 in both diet groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The resting metabolic rates (VO2) of rats fed chow (CH) or a "cafeteria" (CAF) diet of highly palatable human foods were measured at thermoneutrality (28 degrees C) before and shortly after two-thirds hepatectomy or sham operation, and again after administration of propranolol (5 mg/kg). CAF rats initially had a 17% and 1.2 mL/min higher mean resting VO2 than CH rats, a difference usually considered to represent the diet-induced thermogenesis (DIT) that CAF rats develop during overconsumption of the diet. Sham operation did not significantly affect resting VO2 in either diet group. Two-thirds hepatectomy decreased VO2 by about 1.0 mL/min more (125% more) in CAF rats than in CH rats, from which it may be estimated that the CAF rats initially had a liver VO2 about 1.6 mL/min higher than that of the CH rats, a difference more than sufficient to fully account for their apparent DIT. Propranolol did not significantly affect the VO2 of CH rats. It reduced the VO2 of sham-operated CAF rats by 0.94 +/- 0.08 mL/min (12%), but had a significantly smaller effect (delta VO2 = -0.50 +/- 0.05 mL/min) in partially hepatectomized CAF rats. This difference suggests that about 70% of the propranolol-inhibitable fraction of the elevated VO2 of the CAF rats, presumably a measure of sympathetically mediated DIT, resided in the liver. This study thus points to the liver as the major (70-100%) effector of the DIT of CAF rats.