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Glycemic index, glycemic load, and colorectal cancer risk stratified by insulin receptor expression: the Japan Public
Yuki Homma1,2, Shiori Nakano1, Kenshiro Nishihara1,3
1Division of Epidemiology, National Cancer Center Institute for Cancer Control, Tokyo, Japan.
Purpose:
Glycemic index (GI) and glycemic load (GL) are markers for postprandial glucose level. Since insulin, a hormone secreted to control hyperglycemia, is likely to promote the progression of tumor cells, the association between GI/GL and risk of colorectal cancer (CRC) has been researched for decades but still remains controversial. This study investigated the association between GI/GL and CRC risk, considering subtypes based on insulin receptor beta (IRβ) expression.
Methods:
In a large-scale, population-based prospective cohort study involving 18,537 Japanese participants, a total of 415 CRC cases were evaluated for IRβ expression using immunohistochemistry. GI and GL were calculated using a validated food frequency questionnaire. The Cox proportional hazards model was used to assess the hazard ratios (HRs) and 95% confidence intervals (CIs) of the risk of CRC and its specific subtypes. Additionally, we conducted sensitivity analyses to confirm the robustness of the results.
Results:
No significant associations were observed between dietary GI, GL and overall CRC risk. Further, no significant associations were detected in IRβ-stratified analyses. The heterogeneities in the associations by IRβ status were also not statistically significant. (GI: p for heterogeneity 0.83 for men and 0.96 for women; GL: p for heterogeneity 0.84 for men and 0.60 for women) Sensitivity analyses yielded robust results.
Conclusions:
This study did not observe a significant association between GI/GL and overall CRC or IRβ-defined subtypes. These results, particularly those from the assessment of IRβ status, do not support a possible association between GI/GL and CRC development.
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