Postprandial Endotoxemia Increases with Fat Amount in Obese Men: Inflammatory Impact of LPS Handling

Abstract

Objectives: LPS, so‐called endotoxins, are now recognized as a triggering factor of the low‐grade inflammation observed in obesity. Recent findings revealed that digestion of a lipid‐rich meal induces a postprandial endotoxemia contributing to increased metabolic risk. However, the possible nutritional modulation of postprandial endotoxemia by various fat amounts remains largely unknown in humans, especially regarding the impact of BMI.
Methods: Normal‐weight (NW) and obese men ingested meals containing 10g or 40g fat. Endotoxemia was measured in plasma and chylomicrons during 8h, together with inflammatory mediators and LPS transporters.
Results: Chylomicrons increased in all subjects according to ingested fat amount ( P <0.01), but only obese men had higher postprandial endotoxemia after 40g fat ( P <0.05). Their chylomicrons also got more enriched with LPS than in NW. We observed neither NFkB translocation, nor IL‐6 gene expression in leukocytes, regardless of BMI or meal. In both groups, fat amount did not modify postprandial response of plasma IL‐6. However, postprandial AUC of IL‐6 in obese was higher than in NW subjects ( P <0.05) parallel to their higher fasting LPS‐Binding Protein (LBP, P <0.05). In fact, postprandial AUC of IL‐6 was correlated with LBP ( P <0.01).

Conclusions
Fat amount contributes to modulate postprandial endotoxemia in obese subjects. The further endotoxin handling in plasma through chylomicrons and LPS transporters appears to be critical in driving the acute inflammatory response. This can contribute to the long term low‐grade inflammation, especially for high cardiometabolic risk individuals.