The Wenner-Gren Institute, The Arrhenius Laboratories F3, Stockholm University, Stockholm SE-106 91, Sweden.
J Exp Biol. 2011 Jan 15;214(Pt 2):242-53. doi: 10.1242/jeb.050989.
Alterations in nonshivering thermogenesis are presently discussed as being both potentially causative of and able to counteract obesity. However, the necessity for mammals to defend their body temperature means that the ambient temperature profoundly affects the outcome and interpretation of metabolic experiments. An adequate understanding and assessment of nonshivering thermogenesis is therefore paramount for metabolic studies. Classical nonshivering thermogenesis is facultative, i.e. it is only activated when an animal acutely requires extra heat (switched on in minutes), and adaptive, i.e. it takes weeks for an increase in capacity to develop. Nonshivering thermogenesis is fully due to brown adipose tissue activity; adaptation corresponds to the recruitment of this tissue. Diet-induced thermogenesis is probably also facultative and adaptive and due to brown adipose tissue activity. Although all mammals respond to injected/infused norepinephrine (noradrenaline) with an increase in metabolism, in non-adapted mammals this increase mainly represents the response of organs not involved in nonshivering thermogenesis; only the increase after adaptation represents nonshivering thermogenesis. Thermogenesis (metabolism) should be expressed per animal, and not per body mass [not even to any power (0.75 or 0.66)]. A 'cold tolerance test' does not examine nonshivering thermogenesis capacity; rather it tests shivering capacity and endurance. For mice, normal animal house temperatures are markedly below thermoneutrality, and the mice therefore have a metabolic rate and food consumption about 1.5 times higher than their intrinsic requirements. Housing and examining mice at normal house temperatures carries a high risk of identifying false positives for intrinsic metabolic changes; in particular, mutations/treatments that affect the animal's insulation (fur, skin) may lead to such problems. Correspondingly, true alterations in intrinsic metabolic rate remain undetected when metabolism is examined at temperatures below thermoneutrality. Thus, experiments with animals kept and examined at thermoneutrality are likely to yield an improved possibility of identifying agents and genes important for human energy balance.
目前认为非颤抖性产热的改变既是肥胖的潜在原因，也能对抗肥胖。然而，哺乳动物必须保护体温，这意味着环境温度会深刻影响代谢实验的结果和解释。因此，充分理解和评估非颤抖性产热对于代谢研究至关重要。经典的非颤抖性产热是适应性的，即只有当动物急需额外热量时才会被激活（几分钟内开启），而且是适应性的，即需要数周时间才能增加产能。非颤抖性产热完全归因于棕色脂肪组织的活性；适应对应于该组织的募集。饮食诱导的产热可能也是适应性的，归因于棕色脂肪组织的活性。虽然所有哺乳动物对注射/输注去甲肾上腺素（去甲肾上腺素）的反应都是代谢增加，但在未适应的哺乳动物中，这种增加主要代表了非颤抖性产热不涉及的器官的反应；只有适应后的增加才代表非颤抖性产热。产热（代谢）应按动物个体表示，而不是按体重[甚至不是任何幂（0.75 或 0.66）]。“耐寒性测试”不检查非颤抖性产热能力；而是测试颤抖能力和耐力。对于老鼠，正常的动物房温度明显低于热中性，因此老鼠的代谢率和食物消耗比其内在需求高 1.5 倍左右。在正常的动物房温度下饲养和检查老鼠会增加识别内在代谢变化的假阳性风险；特别是，影响动物绝缘（皮毛）的突变/治疗可能会导致此类问题。相应地，当代谢在低于热中性的温度下进行检查时，内在代谢率的真正变化仍未被检测到。因此，在热中性条件下饲养和检查动物的实验可能会提高识别对人类能量平衡重要的药物和基因的可能性。
