Hepatic Fat Content and Liver Enzymes Are Associated with Circulating Free and Protein-Bound Advanced Glycation End Products, Which Are Associated with Low-Grade Inflammation: The CODAM Study
Abstract
Advanced glycation end products (AGEs) accumulate in fatty livers and may contribute to low-grade inflammation (LGI), potentially via their receptor, RAGE. It is unknown if the AGE accumulation in fatty livers results in elevated circulating AGEs. In a cohort study, we investigated the association of liver fat and hepatocellular damage with circulating AGEs and soluble RAGE (sRAGE) and subsequently the association of circulating AGEs and sRAGE with LGI. Cross-sectional associations of liver fat percentage (eLF%; ln-transformed) and liver enzymes (LE score; standardized) with circulating AGEs (free CML, CEL, and MG-H1 in nM and protein-bound CML, CEL, and pentosidine in nmol/mmol lysine; ln-transformed) and sRAGE (pg/ml, ln-transformed) and additionally of AGEs and sRAGE with LGI (standardized) were determined by multiple linear regression. eLF% was positively associated with circulating free CEL (β = 0.090; 95% CI 0.041; 0.139) but inversely with protein-bound CML (β = −0.071; 95% CI -0.108; -0.034). Similarly, the LE score was positively associated with free CML (β = 0.044; 95% CI 0.012; 0.076) and CEL (β = 0.040; 95% CI 0.009; 0.072) but inversely with protein-bound CML (β = −0.037; 95% CI -0.060; -0.013). Free CML (β = 0.297; 95% CI 0.049; 0.545) was positively associated with LGI, while protein-bound CML (β = −0.547; 95% CI -0.888; -0.207) was inversely associated, although this association was absent after adjustment for BMI. eLF% and LE score were not associated with…
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Evidence Hub reads this as a cross-sectional. Its evidence level is 4 of 5 (Low · observational). Observational designs can show an association but not prove cause.
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