What is it about?
Deepening insulin resistance leads to the defect of estrogen synthesis and signaling, while low estrogen level or estrogen receptor defect inhibits cellular glucose uptake. Estrogen signal drives and controls all steps of cellular glucose uptake, while a defect of estrogen leads to thorough cellular defects including failure of glucose uptake.
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Why is it important?
Patients with insulin resistance and/or with estrogen signaling defect may be treated by insulin sensitizers and/or exogenous estrogen (oral contraceptive, postmenopausal hormone replacement) for the prevention of cancer development. Moreover, higher estrogen doses are effective even against advanced cancers.
Perspectives
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This page is a summary of: Interplay Between Insulin Resistance and Estrogen Deficiency as co- Activators in Carcinogenesis, Pathology & Oncology Research, October 2011, Springer Science + Business Media,
DOI: 10.1007/s12253-011-9466-8.
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