Title
Insulin resistance and endometrial cancer risk: A systematic review and meta-analysis
Date Issued
01 December 2015
Access level
open access
Resource Type
review
Publisher(s)
Elsevier Ltd
Abstract
Aim It has been suggested that chronic hyperinsulinemia from insulin resistance is involved in the etiology of endometrial cancer (EC). We performed a systematic review and meta-analysis to assess whether insulin resistance is associated with the risk of EC. Methods We searched PubMed-Medline, Embase, Scopus, and Web of Science for articles published from database inception through 30th September 2014. We included all observational studies evaluating components defining insulin resistance in women with and without EC. Quality of the included studies was assessed by Newcastle-Ottawa scale. Random-effects models and inverse variance method were used to meta-analyze the association between insulin resistance components and EC. Results Twenty-five studies satisfied our inclusion criteria. Fasting insulin levels (13 studies, n = 4088) were higher in women with EC (mean difference [MD] 33.94 pmol/L, 95% confidence interval [CI] 15.04-52.85, p = 0.0004). No differences were seen in postmenopausal versus pre- and postmenopausal subgroup analysis. Similarly, non-fasting/fasting C-peptide levels (five studies, n = 1938) were also higher in women with EC (MD 0.14 nmol/L, 95% CI 0.08-0.21, p < 0.00001). Homeostatic model assessment - insulin resistance (HOMA-IR) values (six studies, n = 1859) in EC patients were significantly higher than in women without EC (MD 1.13, 95% CI 0.20-2.06, p = 0.02). There was moderate-to-high heterogeneity among the included studies. Conclusion Currently available epidemiologic evidence is suggestive of significantly higher risk of EC in women with high fasting insulin, non-fasting/fasting C-peptide and HOMA-IR values.
Start page
2747
End page
2758
Volume
51
Issue
18
Language
English
OCDE Knowledge area
Oncología
Scopus EID
2-s2.0-84959494983
PubMed ID
Source
European Journal of Cancer
ISSN of the container
09598049
Sponsor(s)
AVH, VP, VAB-Z, PT, AD and FRP-L declare no relevant competing interests. AD has received research funding from 3M Incorporation .
Sources of information: Directorio de Producción Científica Scopus