期刊
METABOLITES
卷 11, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/metabo11110726
关键词
body fatness; prostate cancer; biomarker; insulin; insulin signalling; mechanisms; systematic review
资金
- World Cancer Research Fund International [WCRF 2015/1421]
- Cancer Research UK [C18281/A29019]
- Integrative Cancer Epidemiology Programme
- NIHR Biomedical Research Centre at University Hospitals Bristol
- Weston NHS Foundation Trust
- University of Bristol
- NIHR Applied Research Collaboration West at University Hospitals Bristol
Reducing body fatness may improve insulin sensitivity, but current evidence is insufficient to support its impact on reducing the risk of PCa. More high-quality evidence is needed to determine whether reducing body fatness can lower PCa risk through the insulin signalling pathway.
Excess body weight is thought to increase the risk of aggressive prostate cancer (PCa), although the biological mechanism is currently unclear. Body fatness is positively associated with a diminished cellular response to insulin and biomarkers of insulin signalling have been positively associated with PCa risk. We carried out a two-pronged systematic review of (a) the effect of reducing body fatness on insulin biomarker levels and (b) the effect of insulin biomarkers on PCa risk, to determine whether a reduction in body fatness could reduce PCa risk via effects on the insulin signalling pathway. We identified seven eligible randomised controlled trials of interventions designed to reduce body fatness which measured insulin biomarkers as an outcome, and six eligible prospective observational studies of insulin biomarkers and PCa risk. We found some evidence that a reduction in body fatness improved insulin sensitivity although our confidence in this evidence was low based on GRADE (Grading of Recommendations, Assessment, Development and Evaluations). We were unable to reach any conclusions on the effect of insulin sensitivity on PCa risk from the few studies included in our systematic review. A reduction in body fatness may reduce PCa risk via insulin signalling, but more high-quality evidence is needed before any conclusions can be reached regarding PCa.
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