From the article:
“Premenopausal women exhibit enhanced insulin sensitivity and reduced incidence of Type 2 diabetes compared with age-equivalent men,” he explained. “But this advantage disappears after menopause with disrupted glucose homeostasis, in part owing to a reduction in circulating estrogen.”
[…]
“We wanted to understand the mechanism by which estrogen regulates gluconeogenesis by means of interaction with hepatic Foxo1,” he explained. “Foxo1 has an important role in the regulation of glucose production through insulin signaling. It is an important component of insulin-signaling cascades regulating cellular growth, differentiation and metabolism.”
He said in both male and ovariectomized female control mice, a subcutaneous estrogen implant improved insulin sensitivity and suppressed gluconeogenesis. However, the estrogen had no effect on the liver-specific Foxo1 knockout mice of both sexes.
“This suggests Foxo1 is required for estrogen to be effective in suppressing gluconeogenesis,” he said.
“We further demonstrated that estrogen suppresses hepatic glucose production through activation of estrogen receptor signaling, which can be independent of insulin receptor substrates Irs1 and Irs2. This reveals an important mechanism for estrogen in the regulation of glucose homeostasis.”
Guo said study results support the hypothesis that improvement of glucose homeostasis by estrogen is regulated by hepatic Foxo1-mediated gluconeogenesis rather than by promoting muscle glucose uptake.
[…]
Guo also noted some foods, such as soybeans, contain a certain amount of phytoestrogens, which can function in a similar way to that of estrogen, regulating bodily glucose metabolism and insulin sensitivity.