Physiology and Behavior Laboratory, Department of Health Sciences and Technology, ETH Zurich, 8603 Schwerzenbach, Switzerland; Institute of Anatomy, University of Zurich, 8057 Zurich, Switzerland.
Institute of Evolutionary Medicine, Medical Faculty, University of Zurich, 8057 Zurich, Switzerland; Biological Anthropology and Comparative Anatomy Unit, University of Adelaide, Adelaide 5005, Australia.
Cell Metab. 2016 Jun 14;23(6):971-979. doi: 10.1016/j.cmet.2016.05.002.
Diet-induced thermogenesis (DIT) has often been argued to be a physiological defense against obesity, but no empirical proof of its effectiveness in limiting human body weight gain is available. We here propose an immune explanation of DIT-i.e., that it results from the coevolution of host and gut microbiota (especially Firmicutes) that ferment ingested food and proliferate, causing periodic, vagally mediated increases in thermogenesis aimed at curtailing their expansion. Because of this evolutionary adaptive significance related to the immune system, DIT is not effective as an "adaptation" to maintain a certain body mass. Were DIT an effective adaptation to prevent obesity, the current obesity epidemic might not have occurred.
饮食诱导产热（DIT）常被认为是一种对抗肥胖的生理防御机制，但目前还没有证据表明其在限制人体体重增加方面的有效性。我们在这里提出了一种关于 DIT 的免疫解释，即它是由宿主和肠道微生物群（特别是厚壁菌门）共同进化而来的，这些微生物群发酵摄入的食物并增殖，导致周期性的、通过迷走神经介导的产热增加，目的是限制它们的扩张。由于这种与免疫系统相关的进化适应性意义，DIT 作为一种“适应”来维持一定的体重并不是有效的。如果 DIT 是一种有效的适应机制来预防肥胖，那么目前的肥胖流行可能就不会发生。
