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

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