A chronic LPS-induced low-grade inflammation fails to reproduce in lean mice the impairment of preference for oily solution found in diet-induced obese mice

Biochimie. 2019 Apr;159:112-121. doi: 10.1016/j.biochi.2018.08.004. Epub 2018 Aug 10.

Abstract

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.

Keywords: Diet-induced obesity; Food choice; Inflammation; Lipids; Lipopolysaccharides.

MeSH terms

  • Animals
  • Behavior, Animal / drug effects*
  • Dietary Fats / adverse effects*
  • Dietary Fats / pharmacology
  • Endotoxemia* / chemically induced
  • Endotoxemia* / metabolism
  • Endotoxemia* / pathology
  • Endotoxemia* / physiopathology
  • Inflammation / chemically induced
  • Inflammation / metabolism
  • Inflammation / pathology
  • Inflammation / physiopathology
  • Lipopolysaccharides / toxicity*
  • Mice
  • Obesity* / chemically induced
  • Obesity* / metabolism
  • Obesity* / pathology
  • Obesity* / physiopathology
  • Transcriptome / drug effects*

Substances

  • Dietary Fats
  • Lipopolysaccharides