Diet-induced obesity (DIO) is associated with a decreased oral fat detection in rodents. This alteration has been explained by an impairment of the lipid-mediated signaling in taste bud cells (TBC). However, factors responsible for this defect remain elusive. Diet rich in saturated fatty acids is known to elicit a metabolic inflammation by promoting intestinal permeation to lipopolysaccharides (LPS), Gram-negative bacteria-derived endotoxins. To determine whether a local inflammation of the gustatory tissue might explain the obese-induced impairment of the oro-sensory detection of lipids, mice were subjected to a DIO protocol. Using a combination of behavioral tests, transcriptomic analyses of gustatory papillae and biochemical assays, we have found that i) DIO elicits a pro-inflammatory genic profile in the circumvallate papillae (CVP), known to house the highest density of lingual taste buds, ii) NFkB, a key player of inflammatory process, might play a role in this transcriptomic pattern, iii) plasma LPS levels are negatively correlated with the preference for oily solution, and iv) a chronic infusion of LPS at a level similar to that found in DIO mice is not sufficient to alter the spontaneous preference for fat in lean mice. Taken together these data bring the demonstration that a saturated high fat diet elicits an inflammatory response at the level of peripheral gustatory pathway and a LPS-induced low-grade endotoxemia alone does not explain the change in the preference for dietary lipids observed in DIO mice.

饮食引起的肥胖症（DIO）与啮齿类动物减少的口服脂肪检测有关。味蕾细胞（TBC）中脂质介导的信号转导受损已解释了这种变化。但是，导致该缺陷的因素仍然难以捉摸。众所周知，富含饱和脂肪酸的饮食会通过促进肠道对脂多糖（LPS）（革兰氏阴性细菌衍生的内毒素）的渗透而引起代谢炎症。为了确定味觉组织的局部炎症是否可以解释肥胖症对脂质的口感检测的损害，对小鼠进行了DIO方案。结合行为测试，味觉乳头的转录组分析和生化分析，我们发现i）DIO引起周缘乳头（CVP）的促炎性基因谱，已知其拥有最高密度的舌味味蕾，ii） NFkB是炎症过程的关键参与者，可能在这种转录组模式中起作用，iii）血浆LPS水平与对油性溶液的偏好负相关，并且iv）以类似于DIO小鼠中发现的水平长期注入LPS不足以改变瘦小鼠中对脂肪的自发偏好。综合这些数据，可以证明饱和的高脂饮食在周围味觉通路水平上会引起炎症反应，而LPS诱导的低度内毒素血症本身并不能解释DIO小鼠对饮食脂质的偏好变化。