Metformin inhibits the mitochondrial respiratory chain in the liver, leading to activation of AMPK, enhancing insulin sensitivity for type 2 diabetes research. Metformin can cross the blood-brain barrier and triggers autophagy[2]. A short-term administration of metformin strongly protected the myocardium against isoproterenol-induced infarction[3]. Metformin decreased glycogen synthesis in a dose-dependent manner with an IC50 value of 196.5 mM. Moreover, a strong inhibition (62%) of glucose produced from lactate/pyruvate (3 mm/0.3 mm) was observed in cells treated with 350 mM metformin[4]. A potential anti-tumourigenic effect of metformin may be mediated by its role in activating AMPK, which in turn inhibits mammalian target of rapamycin (mTOR) [5]. Metformin inhibits cell growth via AMPK activation and subsequent inhibition of PI3K/AKT signaling in A-ESCs (adenomyotic endometrial stroma cells), particularly during the secretory phase, suggesting a greater effect of metformin on A-ESCs from secretory phase[6].
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