The Association of Fried Meat Consumption With the Gut Microbiota and Fecal Metabolites and Its Impact on Glucose Homoeostasis, Intestinal Endotoxin Levels, and Systemic Inflammation: A Randomized Controlled-Feeding Trial
This randomized controlled-feeding trial aimed to determine the impact of fried meat intake on the gut-microbiota and fecal cometabolites and whether such impacts influenced host glucose homoeostasis, intestinal endotoxin levels and systemic inflammation.
Methods
117 overweight adults were randomized into two groups. Fifty-nine participants were provided fried meat 4 times per-week, and fifty-eight participants were restricted from fried meat intake, while holding food group and nutrient compositions constant, for 4 weeks. The gut-microbiota was analyzed by 16S rRNA sequencing. Glucose and insulin concentrations at 0, 30, 60 and 120 min of an oral glucose tolerance test(OGTT), fecal microbiota-host cometabolite levels, and intestinal endotoxin and inflammation serum biomarker levels were measured. The area under the curve (AUC) for insulin, insulinogenic-index(IGI) and muscle insulin resistance index(MIRI) were calculated.
Results
The participants who consumed fried meat had lower IGI values than the controls, but they had higher MIRI and AUC values of insulin and lipopolysaccharide, TNF-α, IL-10 and IL-2 levels(P<0.05). Fried meat intake lowered microbial community richness and decreased Lachnospiraceae and Flavonifractor abundances while increasing Dialister, Dorea and Veillonella abundances(P-FDR<0.05), provoking a significant shift in the fecal cometabolite profile, with lower 3-indolepropionic acid, valeric acid and butyric acid concentrations and higher carnitine and methylglutaric acid concentrations(P-FDR<0.05). Changes in these cometabolite levels were significantly associated with changes in IGI and MIRI values and lipopolysaccharide, FGF21, TNF-α, IL-2 and IL-10 levels(P<0.05).
Conclusions
Fried meat intake impaired glucose homoeostasis and increased intestinal endotoxin and systemic inflammation levels by influencing the gut-microbiota and microbial-host cometabolites.
