Title: ASSOCIATION BETWEEN ADIPONECTIN, INSULIN RESISTANCE, AND ENDOMETRIAL CANCER Authors
|Soliman, Pamela - M D ANDERSON CANCER CE|
|Wu, Diana - M D ANDERSON CANCER CENTE|
|Tortolero-Luna, Guillermo - M D ANDERSON CANCER CENTE|
|Schmeler, Kathleen - M D ANDERSON CANCER CENTE|
|Slomovitz, Brian - M D ANDERSON CANCER CENTE|
|Gershenson, David - M D ANDERSON CANCER CENTE|
|Lu, Karen - M D ANDERSON CANCER CENTE|
Submitted to: CANCER
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 19, 2005
Publication Date: April 25, 2006
Citation: Soliman, P.T., Wu, D., Tortolero-Luna, G., Schmeler, K.M., Slomovitz, B.M., Bray, M.S., Gershenson, D.M., Lu, K.H. 2006. Association between adiponectin, insulin resistance, and endometrial cancer. Cancer. 106:2376-2381. Interpretive Summary: Obesity is associated with reproductive cancers, but body weight is not the only factor in the development of these diseases. Resistance to the effect of insulin may also contribute to an increased risk for these cancers. Adiponectin is a protein secreted by fat cells that is a marker for insulin resistance, with low levels of adiponectin associated with higher levels of insulin resistance. In this study, we tested to see if adiponectin levels were associated with reproductive cancer. We found that average adiponectin levels were significantly lower among people with cancer compared to those without cancer, even after accounting for age, body fatness, diabetes, and high blood pressure. This study suggests that adiponectin and insulin resistance are directly related to the development of reproductive cancer.
Technical Abstract: BACKGROUND: Obesity is a well-known risk factor for the development of endometrial cancer; however, weight alone does not account for all cases. The authors hypothesized that insulin resistance also contributes to an increased risk for endometrial cancer. Adiponectin is a protein secreted by adipose cells and has been shown to be a surrogate marker for insulin resistance, with low levels of adiponectin correlated with hyperinsulinemia and degree of insulin resistance. The purpose of the current study was to determine whether there was an independent association between adiponectin level and endometrial cancer. METHODS: A case-control study was performed on 117 endometrial cancer patients (cases) and 238 women with no history of cancer (controls). Serum adiponectin levels were measured using enzyme-linked immunoadsorbent assay and examined for their association with endometrial cancer. Univariate and multivariate logistic regression analyses were performed, with adjustment for confounding factors. RESULTS: The mean serum adiponectin levels were significantly lower among cases (88.8+/-63.3 ng/mL) than among controls (148.2+/-68.3; P<.001). This inverse correlation continued to be observed after controlling for age, body mass index, diabetes, and hypertension. Cases were significantly more likely to have serum adiponectin levels in the lowest (odds ratio [OR] of 10.5; 95% confidence interval [95% CI], 4.49-24.57 [P<.001]) and intermediate tertiles (OR of 2.5; 95% CI, 1.01-6.21 [P=.05]) when compared with controls. CONCLUSIONS: Adiponectin level was found to be independently and inversely associated with endometrial cancer. Women with endometrial cancer were more likely to have low adiponectin levels than controls, even after adjusting for body mass index. This suggested that insulin resistance is independently associated with endometrial cancer.