Supplementary Material for: A Pilot Study to Evaluate the Role of Obesity and Genetic Variants in Serum C-Reactive Protein Response to an Acute Fructose Load

33Introduction: Excess fructose intake has been linked to increased risk for dyslipidemia, insulin, 34resistance, hyperuricemia, inflammation, and obesity. In this human study, we investigated if serum 35CRP concentrations change after fructose consumption, and whether genetic variants and 36obesity status influences this change. Methods: Blood was drawn before and at four time points 37after administration of a fructose load (n=57). Serum concentrations of CRP were measured, 38and 11 single nucleotides polymorphisms (SNPs) (rs1205, rs1417938, rs1470515, rs3093068, 39 rs6588158, rs16842568, rs2259820, rs157581, rs2794521, rs3093062, rs17700633), 40previously associated with serum CRP were genotyped and assessed for their association with 41CRP levels. Results: Participants identifying as White (n = 37) had higher mean CRP levels across 42all time points compared to those identifying as Black (n = 20). Participants with obesity (BMI ≥ 30 43kg/m2) (n = 25) were younger and had higher mean CRP levels throughout the study period 44compared to those without (n = 32). All SNPs were in Hardy-Weinberg Equilibrium and their 45effect allele frequencies ranged between 11and 96%. Baseline CRP was associated with CRP 46SNPs rs1417938 and rs2794521 (p <0.005), with rs2794521 also associated with CRP response to 47fructose challenge (p < 0.005). The variability in responses to fructose and genetic associations 48were mainly observed in individuals without obesity. Obesity status was associated with early 49changes in CRP (0-30 min and 30-60min) whereas CRP SNPs were associated with later changes 50(60-120min and 120-180 min). Conclusion: Changes in serum CRP were associated with obesity 51 status or SNPs based on the time elapsed since fructose ingestion. Larger studies are needed to 52 confirm and validate these associations. 53 54