Table 2.

Examples of effects of food intake and particularly effects of high-fat diet on intestinal barrier function

Author/Ref. #	Sample	Treatment/Duration	Main Results	Comment
Amar et al., ref. 34; Cani et al., ref. 35	1,015 healthy people randomly recruited in France	3-day food record; plasma LPS tested in 201 male participants	Association between food intake (positively correlated with fat intake) and plasma LPS.	Experimental data in mice suggest that fat was more efficient in transporting bacterial LPS from the intestinal lumen into the bloodstream.
Lyte et al., ref. 36	20 healthy adults (mean age 25±3.2 years)	Control diet (olive oil - 20%) HFD with omega-3 (fish oil, 35%) HFD with omega-6 (grape seed oil, 35%) Diet rich in saturated fat (coconut oil, 35%)	Serum endotoxin concentration increased during postprandial period after consumption of a high-saturated fat meal, but decreased after the meal with n-3	The n-6 meal did not affect postprandial endotoxin concentration in relation to the control meal. There was no postprandial effect on inflammatory biomarkers after meals.
Bowser et al., ref. 37	13 normal weight and sedentary adult males (mean age 22.2±1.6 years); all weight stable	2-week control diet [55% CHO, 30% fat (9% saturated), and 15% protein]; HFD for 5 days [55% fat (25% saturated fat), 30% CHO, and 15% protein]; HFM challenge [820 kcal: 25% CHO, 12% protein, 63% fat (~26% saturated fat)] before and following the 5-day HFD	No significant changes in gastroduodenal, small intestinal (p=0.084 LM ratio), or colonic permeability following HFD.	Fasting endotoxin concentrations increased (1.2±0.1 vs. 2.3±0.4 Eu/mL, p=0.04) following HFD, but postprandial serum endotoxin concentrations area under the curve did not change following HFD.

CHO=carbohydrate; HFD=high fat diet; HFM=high fat meal; LM ratio=lactulose to mannitol ratio; LPS=lipopolysaccharides