Adaptive Thermogenesis Is Intact in B6 and A/J Mice Studied at Thermoneutrality

We determined the influence of thermonuetrality on the oxygen consumption (VO2) and heart rate (HR) responses to short-term moderate fat feeding in male C57BL/6J (B6; obesity-prone) mice and A/J (obesity-resistant) mice. Mice were adapted to either Ta=23°C or Ta=30°C for at least 5 weeks, implanted with telemetry devices, and housed in metabolic chambers for measurement of food intake, VO2, HR, mean arterial pressure (MAP), and locomotor activity. Access to moderate fat diet resulted in similar increases in normalized VO2 at both Ta=23°C (B6 Δ: 2.7±0.4 ml/min/kg0.75; A/J Δ: 3.8±0.5 ml/min/kg0.75) and Ta=30°C (B6 Δ: 2.4±0.4 ml/min/kg0.75; A/J Δ: 4.4±0.6 ml/min/kg0.75) within each respective strain. However, the A/J mice (Δ: 4.1±0.4 ml/min/kg0.75) had an enhanced metabolic response compared to the B6 mice (Δ: 2.5±0.3 ml/min/kg0.75). Tachycardia following the nutritional intervention occurred at Ta=30°C, and was similar in magnitude in B6 mice (Δ: 55±10 beats/min at Ta=30°C vs. 12±8 beats/min at Ta=23°C) and A/J mice (Δ: 61 ± 15 beats/min at Ta=30°C vs. 25±18 beats/min at Ta=23°C). By the third day of access to moderate fat diet, caloric intake for A/J mice returned to baseline chow levels. However, the B6 mice remained hyperphagic throughout the 7 days of moderate fat feeding. The results demonstrate that an enhanced ability to engage adaptive thermogenesis is one mechanism utilized by the A/J mice to prevent obesity. Because the thermogenic response was observed in mice chronically adapted to thermoneutrality, we conclude it is not likely mediated by brown adipose tissue. Finally, the observation that the cardiovascular responses to short term moderate fat feeding in mice were more evident at thermoneutrality suggests that rodent studies examining the role of obesity on cardiovascular disease should be performed at thermoneutral temperatures.