DeRuisseau L R, Parsons A D, Overton J M
Department of Nutrition, Food, and Exercise Sciences, Florida State University, Tallahassee, FL 32306-4340, USA.
Metabolism. 2004 Nov;53(11):1417-23. doi: 10.1016/j.metabol.2004.06.007.
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.
为了研究肥胖抵抗机制，我们在环境温度（Ta）=23℃和热中性温度（Ta = 30℃）条件下，对肥胖易感（B6）或肥胖抵抗（A/J）小鼠进行了短期适度脂肪喂养的生理反应研究。我们假设A/J小鼠对中等脂肪饮食的摄入会表现出更强的适应性产热反应，并且由于棕色脂肪组织（BAT）活性降低，这种反应在热中性条件下会减弱。将B6和A/J小鼠分别适应于Ta = 23℃或Ta = 30℃，植入遥测设备，饲养在代谢室中以测量食物摄入量、耗氧量（Vo₂）和心率（HR），并在食用含32%热量来自脂肪的饮食的1周前后进行研究。食用32%脂肪饮食导致两种品系的热量摄入增加，但A/J小鼠的热量摄入在72小时内恢复到基线水平，而B6小鼠仍处于食欲亢进状态。两种品系在光照期的Vo₂均增加，表明存在适应性产热；然而，在为期1周的喂养试验中，光照期的Vo₂在品系间没有差异。令人惊讶的是，Ta对两种小鼠品系的饮食诱导产热均无影响。适度的高脂肪喂养会导致轻度心动过速，B6和A/J小鼠相似，在热中性条件下更明显。我们得出结论，在热中性条件下研究的两种小鼠品系中，适应性产热反应均完整，这表明BAT在对摄食过多的初始代谢反应中作用最小。此外，结果表明，热量摄入控制的差异而非适应性产热能力的差异可能导致A/J和B6小鼠对肥胖的相对易感性。
