Hormonal
Estrogen (17β-estradiol) improves insulin sensitivity and suppresses hepatic gluconeogenesis by activating the ERα-PI3K-Akt-Foxo1 signaling pathway, thereby reducing fasting blood glucose levels.
In preclinical models, estrogen improves blood sugar control by telling the liver to stop producing excess glucose. This happens through a specific signaling pathway involving ERα and Foxo1. This suggests that maintaining healthy estrogen levels or targeting this specific liver pathway could be a strategy for managing glucose metabolism, particularly in postmenopausal women or those with estrogen deficiency.
Here, we investigated the action of E2 on glucose homeostasis... subcutaneous E2 implant improved insulin sensitivity and suppressed gluconeogenesis... E2 suppresses hepatic gluconeogenesis through activation of (ER)a–phosphoinositide 3-kinase–estrogen receptor Akt–Foxo1 signaling
Why this rating
High-quality mechanistic evidence using multiple mouse models (WT, L-F1KO, L-DKO, S253A) and primary hepatocytes, though results are preclinical.
Source
Estrogen Improves Insulin Sensitivity and Suppresses Gluconeogenesis via the Transcription Factor Foxo1
Hui Yan et al. · Diabetes · 2018
DOI 10.2337/db18-0638
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