Zusammenfassung
Objective: Adipositas and insulin resistance are modifiable risk factors for breast cancer. Adiponectin seems to be an important linkage of these associations. In this study, we investigated the relationship between intratumoral adiponectin receptor expression and insulin resistance as well as intratumoral insulin/IGF receptor expression in breast cancer specimen. Methods: Breast cancer tissue ...
Zusammenfassung
Objective: Adipositas and insulin resistance are modifiable risk factors for breast cancer. Adiponectin seems to be an important linkage of these associations. In this study, we investigated the relationship between intratumoral adiponectin receptor expression and insulin resistance as well as intratumoral insulin/IGF receptor expression in breast cancer specimen. Methods: Breast cancer tissue and fasting serum were collected from 26 female patients. After microdissection of frozen samples, RNA was isolated and expression of insulin receptor, IGFR1, IGFR2, AdipoR1 and AdipoR2 was measured on mRNA level by means of real time RT-PCR. Fasting insulin, glucose and c-peptide serum levels were analysed by ELISA. Insulin resistance was calculated using the HOMA model. Results: We were able to confirm AdipoR1 and AdipoR2 expression, respectively, in breastcancer specimen. Actually, neither insulin serum level nor whole-body insulin resistance showed any effect on insulin/IGF or adiponectin receptor expression in breast cancer. A strong positive correlation between insulin as well as IGF1 receptor and AdipoR1, but not AdipoR2, expression could be observed. Interestingly, AdipoR2 expression significantly correlated with vascular and lymphovascular invasion of breast cancer. Conclusion: We propose a close relationship between the intratumoral insulin signalling system and AdipoR1 but not AdipoR2 expression. As AdipoR2 but not AdipoR1 expression seems to correlate with invasiveness, we assume different functions of the two adiponectin receptors in breast cancer. (C) 2009 Published by Elsevier Ireland Ltd.