Diabetes & Endocrinology

Oestradiol likely to cause type 2 diabetes in women of menopausal age

A cross-sectional analysis, as described in the Journal of Diabetes, has revealed that the main female hormone, 17β-estradiol (E2) is affiliated with the risk of type 2 diabetes (T2D). However, this association between E2 and T2D is independent of adiposity or insulin resistance.


17β-estradiol (E2), also known as oestradiol, plays a significant role in the regulation of estrous and menstrual female reproductive cycles. A systematic meta-analysis of healthy postmenopausal women who were free of T2D at borderline was done. These women were taken as a sample in the study for a period of 11 years. The women were untreated and had low circulating E2 concentrations. Thirteen studies were done in which the researchers examined the relationship between the sex hormone-binding globulin (SHBG) and T2D risk in these women. The study reported lower levels of SHBG and higher levels of total E2 were related to increased risk of T2D.


This study was independent of the known risk factors of T2D which include body mass index and insulin resistance. However, researchers did not find any association between T2D risk and testosterone. These results, nonetheless, were not an assay artifact due to their generalization. The examination did not use mass spectrometry, which is the most reliable technology that is used for steroid evaluation.


Despite of the generalization, this research has opened doors to new questions such as is E2, that is being circulated by SHBG, influential in predisposing postmenopausal women to T2D or is it a new indirect biomarker of the pathological process to T2D in postmenopausal women.


The answer to the first question is most likely no, since women who were given the menopausal treatment with estrogens consistently showed decreased T2D incidence. These trials were large, randomized and controlled. Also, previous studies in preclinical models concluded that therapeutic doses of E2 and other estrogens improved glucose homeostasis but there was no beneficial effect observed. However, it did show that high doses of oral estrogens or high serum concentrations of endogenous E2 such as those seen during pregnancy and in transexuals, produced insulin resistance.


In addition, the study also showed that there was no relation between E2 and T2D in premenopausal women, who exhibit higher circulating E2 concentrations. And lastly, the cohort study concluded that early menopause that led to more prolonged E2 deficiency was associated with a greater risk of T2D.
Further studies are required to provide an evaluation that will determine the correct measures of cellular estrogen biosynthesis and its sensitivity in the pathological process that predisposes T2D as well as the association of E2 with other chronic diseases.

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