The Role of Insulin Resistance in Benign Breast Disease

Main regulators of breast metabolism are estradiol, progesterone, prolactin, growth hormone, and insulin-like growth factor 1 (IGF-1) [1]. They control cell function, proliferation, and differentiation activating intracellular signaling cascade (Erk, Akt, JNK, and Ark/Stat) of breast tissue [2]. Estrogen receptor (ER) expression in the breast is stable and differs relatively little in correlation with reproductive status, menstrual cycle phase, or exogenous hormones [3]. Estrogens have apocrine, paracrine, and intercrine effects. Receptors for estradiol are present in fibroblast, epithelial cells, adipocytes, and stromal tissue. Intramammary concentration of estradiol is 20 times higher compared to the level in the blood. Estradiol increases number of progesterone receptors, epithelial proliferation in the luteal phase, galactophore differentiation, connective tissue development, and growth hormone.