What is it about?
The primary antihyperglycemic effect of metformin, an oral biguanide and a preferred treatment for type-2 diabetes, is caused by the suppression of hepatic glucose production. Metformin which activates AMP-activated protein kinase (AMPK) and reduces protein synthesis and cell proliferation via suppression of the mTOR. Metformin also increases insulin sensitivity and cellular glucose uptake and thus decreases circulating insulin levels; insulin and insulin-like growth factor (IGF)-1 are known to increase cell proliferation We examined metformin effect both histopathologically and genetically for endometrial hyperplasia treatment
Featured Image
Why is it important?
The data indicate that metformin reduces estrogen-induced EH in rats, via activation of the caspase-dependent mitochondrial apoptotic pathway, to the same degree as progesterone.
Read the Original
This page is a summary of: Induction of apoptosis by metformin and progesterone in estrogen-induced endometrial hyperplasia in rats: involvement of the bcl-2 family proteins, Gynecological Endocrinology, November 2017, Taylor & Francis,
DOI: 10.1080/09513590.2017.1409708.
You can read the full text:
Contributors
The following have contributed to this page







