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 (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)

Increased Energy Expenditure in Gastric Bypass Rats Is Not Caused by Activated Brown Adipose Tissue

“…Our findings are in line with previous reports demonstrating an increased oxygen consumption following feeding in rats which was not accounted for by increased oxygen consumption by interscapular brown adipose tissue [33]. Therefore, other tissues like skeletal muscles or liver being sensitive to adrenergic stimulation may be responsible for the diet-induced increase in oxygen uptake or diet-induced thermogenesis [34], thus further questioning the role of brown adipose tissue in rats [34].…”

Brown and beige fat: development, function and therapeutic potential

“…Notably, previous studies in rats housed at thermoneutrality failed to find any substantial contribution of BAT activity to diet-induced thermogenesis 58 . Moreover, Anunciado-Koza et al 55 did not observe changes in adiposity in their studies of Ucp1 knockout mice when the mice were housed under varying temperature conditions.…”

Immunity-Based Evolutionary Interpretation of Diet-Induced Thermogenesis

“…These findings are not consistent with a lower resting metabolism of UCP1 knockout mice and may be related to differences in the genetic background of the mice as well as in environmental factors, such as raising conditions and a prior period of cold adaptation. Other findings question the significance of BAT in the energy expenditure increase in DIT as well: at both 24 C and 28 C, resting metabolic rate and BAT mass of rats increased significantly after 2 to 3 weeks of cafeteria diet feeding, but oxygen consumption rate of BAT did not increase (Ma et al, 1988), essentially suggesting that BAT-independent thermogenic mechanisms are sufficient to generate the energy expenditure increase accompanying DIO. One contributing mechanism could be increased ventilation.…”