Sai Sravani Vennam, Valentina Talevi, Geethika Venkataraman, Rayyan Ahmed Syed, Xinruo Zhang, Baba B Mass, Venkata Saroja Voruganti
{"title":"A Pilot Study to Evaluate the Role of Obesity and Genetic Variants in Serum C-Reactive Protein Response to an Acute Fructose Load.","authors":"Sai Sravani Vennam, Valentina Talevi, Geethika Venkataraman, Rayyan Ahmed Syed, Xinruo Zhang, Baba B Mass, Venkata Saroja Voruganti","doi":"10.1159/000544832","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":"1-27"},"PeriodicalIF":2.0000,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Lifestyle Genomics","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000544832","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
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. 53 54.
期刊介绍:
Lifestyle Genomics aims to provide a forum for highlighting new advances in the broad area of lifestyle-gene interactions and their influence on health and disease. The journal welcomes novel contributions that investigate how genetics may influence a person’s response to lifestyle factors, such as diet and nutrition, natural health products, physical activity, and sleep, amongst others. Additionally, contributions examining how lifestyle factors influence the expression/abundance of genes, proteins and metabolites in cell and animal models as well as in humans are also of interest. The journal will publish high-quality original research papers, brief research communications, reviews outlining timely advances in the field, and brief research methods pertaining to lifestyle genomics. It will also include a unique section under the heading “Market Place” presenting articles of companies active in the area of lifestyle genomics. Research articles will undergo rigorous scientific as well as statistical/bioinformatic review to ensure excellence.