Adaptive thermogenesis is intact in B6 and A/J mice studied at thermoneutrality.

To investigate mechanisms of resistance to obesity, the physiologic responses to short-term moderate fat feeding were studied at ambient temperature (T(a)) = 23 degrees C and thermonuetrality (T(a) = 30 degrees C) in mice susceptible (B6) or resistant (A/J) to obesity. We hypothesized that A/J mice would exhibit greater adaptive thermogenic responses to consumption of moderate-fat diets, and that this response would be attenuated in thermoneutral conditions due to reduced activity of brown adipose tissue (BAT). B6 and A/J mice were adapted to either T(a) = 23 degrees C or T(a) = 30 degrees C, implanted with telemetry devices, housed in metabolic chambers for measurement of food intake, oxygen consumption (Vo(2)), and heart rate (HR), and studied before and during 1 week of consuming a diet containing 32% of calories from fat. Access to 32% fat diet resulted in increased caloric intake in both strains, but caloric intake for A/J mice returned to baseline levels within 72 hours, while B6 mice remained hyperphagic. Both strains exhibited increased light-phase Vo(2) indicative of adaptive thermogenesis; however, there was no strain difference in light-phase Vo(2) during the 1-week feeding trial. Surprisingly, T(a) had no effect on diet-induced thermogenesis in either mouse strain. Moderate high-fat feeding produced mild tachycardia that was similar in B6 and A/J mice and more clearly evident at thermonuetrality. We conclude that adaptive thermogenic responses are intact in both mouse strains studied at thermoneutrality, suggesting a minimal role for BAT in the initial metabolic response to hyperphagia. Furthermore, the results suggest that differences in control of caloric intake, rather than capacity for adaptive thermogenesis, may contribute to the relative susceptibility to obesity in A/J and B6 mice.