Environmental and Clinical Determinants of Plasma-lipopolysaccharide Binding Protein and Association with Non-Alcoholic Fatty Liver Disease in Older Women (P08-022-19)

Abstract

Objectives Nonalcoholic fatty liver disease (NAFLD) is an increasingly condition seen in patients with obesity predicting cardiovascular mortality. NAFLD ranges from simple steatosis without significant inflammation(90%), to steatohepatitis (10–30%). Growing evidence suggests that either obesity and gut-flora dysbiosis may activate inflammatory signaling pathways in hepatic cells. Both risk factors may be controlled by dietary components. Manipulated and processed foods consumption would lead to intestinal bacterial overgrowth and/or altered mucosal permeability allowing the bacterial lipopolysaccharides (LPS) to activate TNF-a production in Kupffer cells. OBJECTIVE: Following previous finding that food inadequacy is an environmental risk factor for NAFLD, we presently look at the effects of dietary components on the circulating LPS. Methods Baseline data of 74 women (35–67 yrs) were analyzed cross-sectional. Analysis included medical, dietary, anthropometry, and plasma biochemistry. Obesity was diagnosed by BMI values and NAFLD by “fatty liver index” ≥60. Plasma immune-nephelometric assay of us-CRP and ELISA of lipopolysaccharide binding protein (LBP) were used as inflammatory markers. LBP values were split into tertiles for comparison with co-variables. SPSS version 19.0 was used to complete ANOVA and evaluated LBP tertiles (T1-T3) at significance level of P = 0.05. Results Obesity reached 45.9% of the sample and NAFLD, 48.6%. LBP concentrations were significantly higher(T3) in obese and NAFLD women, ingesting high proportion of highly processed diets with high amount of fructose and high sodium/potassium ratio. There was a weak association of higher LBP(T3) with altered us-CRP. Analysis revealed that increased LBP was independently associated with higher intake of fructose and lower polyunsaturated fat, higher glutamic-pyruvic transaminase and higher percentage of body fatness. Conclusions LBP is associated with body fatness and NAFLD connected to dietary refined food(high fructose and low PUFA), probably impacting gut-flora LPS production and/or translocation to liver, activating TLRs and, from there, spreading systemicaly, bound to liver-born LBP. Funding Sources ACKNOWLEDGEMENTS: Brazilian foundations CNPq and CAPES.