Immunity-Based Evolutionary Interpretation of Diet-Induced Thermogenesis  Wan-Hui Liao, Maciej Henneberg, Wolfgang Langhans  Cell Metabolism  Volume 23, Issue 6, Pages 971-979 (June 2016) DOI: 10.1016/j.cmet.2016.05.002 Copyright © 2016 Elsevier Inc. Terms and Conditions

Figure 1 Diet-Induced-Thermogenesis Does Not Defend Against Obesity but Aids the Immune System (1) Thermogenesis induced by chronic high-fat diet or cafeteria diet feeding is likely mediated by Firmicutes bacteria, which dominate the gut microbiota under various conditions, including in young age, in obesity, and during cold exposure (i.e., in situations with the common feature of brown adipose tissue [BAT] activation). (2) Firmicutes bacteria are potential threats to the host because they can compromise the intestinal barrier by downregulating glucagon-like peptide-2 (GLP-2), an intestinal tight junction controller, leading to bacteremia and bacterial toxin entry, thus promoting the progression of metabolic sequelae commonly associated with obesity. (3) By detecting the reduction in gut content pH and the heat with TRPV-1 receptors, vagal afferents monitor the increasing activity and population growth of Firmicutes bacteria and induce a fever-like response based on the recruitment of BAT and likely also UCP1-independent pathways of heat generation. (4) This diet-induced fever-like host response strengthens gut immunity and mitigates bacterial replication. F: bacteria in the Firmicutes phylum; B: bacteria in the Bacteroidetes phylum. Cell Metabolism 2016 23, 971-979DOI: (10.1016/j.cmet.2016.05.002) Copyright © 2016 Elsevier Inc. Terms and Conditions