Background
Postprandial lipemia stimulates proinflammatory mediators and is a risk factor for cardiovascular disease. Chronic disease and diet are known to influence the gut microbial community in ways that alter the availability of bioactive compounds capable of influencing the host. The purpose of this study was to identify gut microbiome taxa and inflammatory cytokines differentiating individuals with lower and higher postprandial triglyceridemia.
Methods
A high-fat meal (43.1% fat) was given to 40 healthy, overweight and obese adults to assess the serum triglyceride response in the immediate four-hour postprandial period. Participants were categorized into two groups (high and low) based on serum triglyceride responses. We measured blood lipids, inflammatory cytokines, fat mass, visceral adiposity and used 16S rRNA target amplicon sequencing to identify microbial taxa in human fecal samples distinguishing the two groups. The gut microbiome was assessed using unconstrained ordination, followed by a high-dimensional class comparison to determine discriminative microbial features of the postprandial triglyceride response (ppTG).
Results
High ppTG responders had higher body mass index, visceral adiposity, and fasting serum cholesterol levels than low responders and had a decreased postprandial IL-17 response to the high-fat meal. The overall gut microbiome did not cluster by ppTG response but were found to have four discriminative bacterial features between high and low ppTG. Lower relative abundance of Clostridium Cluster XIVa and higher relative abundance of Pasteurellaceae, Alistipes , and Prevotella was observed in low ppTG relative to high ppTG.
Conclusions
Our findings suggest that specific gut microbial taxa involved in short-chain fatty acid production can discriminate the postprandial triglyceride response in overweight and obese adults. These findings may have implications in how we develop microbial therapies and choose to monitor and treat individuals with hypertriglyceridemia or who may have an increased risk of chronic disease.