Deciphering the role of classical oestrogen receptor in insulin resistance and type 2 diabetes mellitus: From molecular mechanism to clinical evidence.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing preclinical mechanisms and clinical trials without systematic review methods
PubMed 40256228 · doi:10.34172/bi.30378
What was done
This narrative review synthesized in vitro, in vivo, and clinical trial evidence examining the role of classical oestrogen receptors (ERα and ERβ) in insulin resistance and type 2 diabetes mellitus (T2DM). The authors evaluated molecular mechanisms—including pancreatic β-cell function, GLUT4 expression, lipid homeostasis, oxidative stress, and inflammatory cascades—and assessed clinical literature on menopausal hormone therapy (MHT) for reducing T2DM risk in menopausal women.
What was found
The abstract reports no quantitative values or effect estimates. Qualitatively, it notes that loss of circulating oestrogen acting through ERα and ERβ impairs pancreatic islet function, GLUT4 expression, insulin sensitivity, and glucose tolerance while exacerbating oxidative stress and inflammation, with these effects reversed by 17β-oestradiol. It also reports that clinical trials indicate protective effects of MHT on glucose metabolism in perimenopausal women, though potential side effects such as obesity and hyperlipidaemia remain concerns.
Why it matters
It outlines the mechanistic pathways connecting estrogen receptor biology to glucose regulation and contextualizes the therapeutic potential of hormone replacement for metabolic dysfunction in postmenopausal women.
Limits
The abstract contains no numerical data, effect sizes, sample sizes, or systematic review methodology. Preclinical findings may not translate directly to humans, and potential metabolic risks associated with estrogen therapy remain insufficiently characterized.
Cited by
- supports The loss of estrogen from the body makes a person more insulin resistant.