Impact of Trans-Fats on Heat-Shock Protein Expression and the Gut Microbiota Profile of Mice

Partially hydrogenated oils are known to cause metabolic stress and dyslipidemia. This paper explores a new dimension about the interaction between dietary trans-fats and the defense heat-shock protein (HSP) system, inflammation, and the gut microbiota of mice consuming a hyperlipidic diet containing partially hydrogenated vegetable oil free of animal fat. Five diet groups were installed: control diet, 2 hyperlipidic-partially hydrogenated-oil diets, each containing either casein or whey-protein hydrolysate (WPH) as protein source, and 2 consuming hyperlipidic-unhydrogenated-oil diets containing either WPH or casein as a protein source. The partially hydrogenated oil inhibited c-Jun NH2-terminal kinase phosphorylation in the casein diets, but without altering -B kinase. Neither the lipid nor the protein had an influence on the proinflammatory toll-like receptor 4 (TLR4) pathway, but the combination of the high-lipid content and WPH impaired glucose tolerance without altering insulin or glucose transporter-4 translocation. It was remarkable to observe that, contrary to the case of a common high-fat diet, the lard-free hyperlipidic diets were hardly able to invert the Bacteroidetes:Firmicutes phylum ratio. Our results suggest that, in the absence of lard, the intake of trans-fatty acids is less harmful than expected because it does not trigger TLR4-inflammation or pose great threat to the normal gut microbiota. WPH had the effect of promoting the expression of HSP90, HSP60, and HSP25, but did not prevent dysbiosis, when the diet contained the unhydrogenated oil. The partially hydrogenated oil also seemed to antagonize the ability of WPH to induce the expression of protective HSPs.