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Main dietary fats in high-fat-diet are saturated fats esp. Very Long Chain Fatty Acids (VLCFAs) and Long chain Fatty Acids (LCFAs). Relevant examples are:
In mice, high-fat diet (HFD) impairs the production of interleukin-22 (IL-22) by group 3 innate lymphoid cells (ILC3s). This impairment was associated with rapid dysbiosis, increased intestinal permeability, and reduced production of antimicrobial peptides, mucus, and tight junction proteins. Saturated fatty acids impair the function of ILC3s, while unsaturated fatty acids promote IL-22 secretion by ILC3s through the formation of lipid droplets using diacylglycerol O-acyltransferase (DGAT) enzymes.
Chronic consumption of High-fat diet (HFD) violates the intestinal barrier integrity. The tight-junction (TJ) tightness is reduced by downregulating the expression of TJ proteins or stimulating aberrant prejunctional-actinomyosin ring (PAR) contraction. Luminal components can thus reach the lamina propria (LP).
High-fat diet (HFD), therefore, changes the gut microbiota composition (dysbiosis). This increases the occurrence of pathogenic strains, such as Desulfovibrio spp., which deconjugate Taurocholate (TCA)-producing genotoxic H2S gas.
The bile acids and Fatty acids translocated in this way induce oxidative stress and apoptosis of the enterocytes, further reducing the tight seal of the lumen.
Furthermore, fatty acid-induced Unfolded protein response (UPR) stress in goblet cells inhibits mucus secretion.
All these factors promote an inflammatory response which furthers the cycle of intestinal barrier degeneration, predisposing the host to gastrointestinal pathologies.
Long-term high-fat diet consumption affects gut microbiota composition in both animal models and humans with a direct influence on short-chain fatty acids (SCFAs) production and host health.
Wellformulated high-fat diets, such as ketogenic diets, may provide healthful alternative fuel sources for the human gut.
see also:
Fatty Acids & Gut microbiota
Very Long Chain Fatty Acids (VLCFAs)