| Literature DB >> 34369225 |
Kelly L Stewart1, Biljana Gigic2, Caroline Himbert3,4, Christy A Warby4, Jennifer Ose3,4, Tengda Lin3,4, Petra Schrotz-King5, Jürgen Boehm3,4, Kristine C Jordan1, Julie Metos1, Martin Schneider2, Jane C Figueiredo6, Christopher I Li7, David Shibata8, Erin Siegel9, Adetunji T Toriola10, Sheetal Hardikar3,4,7, Cornelia M Ulrich3,4.
Abstract
Evidence suggests a positive association between sugar intake and colorectal cancer (CRC) outcomes. We sought to investigate inflammation and angiogenesis as underlying mechanisms behind increased sugar intake and worse CRC outcomes. Pre-surgery serum samples were obtained from 191 patients diagnosed with primary invasive stage I-IV CRC. Biomarkers of inflammation (CRP, SAA, IL-6, IL-8, MCP-1, TNFα) and angiogenesis (VEGFA, VEGFD, sICAM-1 and sVCAM-1) were analyzed (Meso-Scale-Discovery). Fructose, glucose, sucrose, and total sugar intake (calories/day, % total calories) were assessed by FFQ. Pearson's correlation and multiple linear regression analyses were performed. Patients were on average 64 years old, 64% were male, the majority was diagnosed with stage II-III (58%) cancers, and 67% were either overweight or obese. Among normal-weight individuals (BMI <25 kg/m2), we observed a significant inverse association between VEGFD and any type of sugar intake in cal/day (sucrose: p = 0.01, glucose and fructose: p < 0.001) and MCP-1 and fructose intake (p = 0.05). The magnitude of reduction in VEGF ranged between -1.24 for sucrose to 4.49 for glucose intake, and -2.64 for fructose intake for MCP-1 levels. Sugar intake was associated with some inflammation or angiogenesis biomarkers, among CRC patients; differences were observed by adiposity that warrant further investigation.Supplemental data for this article is available online at at 10.1080/01635581.2021.1957133.Entities:
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Year: 2021 PMID: 34369225 PMCID: PMC8825879 DOI: 10.1080/01635581.2021.1957133
Source DB: PubMed Journal: Nutr Cancer ISSN: 0163-5581 Impact factor: 2.816