Estradiol, a steroid hormone, is a crucial regulator of metabolic health in both women and men beyond its known reproductive functions.
It influences energy homeostasis, glucose metabolism, lipid balance, and overall metabolic health through estrogen receptors ERα and ERβ.
ERα activation in hepatic cells by estradiol affects glucose production and lipid synthesis, maintaining glucose homeostasis and preventing fat accumulation.
In adipose tissue, estradiol enhances insulin sensitivity, modulates adipokine secretion, and influences systemic inflammation and energy balance.
Estradiol signaling in skeletal muscle boosts mitochondrial function, improves insulin sensitivity, and enhances energy utilization.
In pancreatic beta cells, estradiol receptor engagement supports cell survival, insulin secretion, and mitigates metabolic stress effects.
Estradiol influences metabolic regulation in the central nervous system, modulating appetite, energy expenditure, and glucose metabolism through ERα and ERβ.
Postmenopausal decline in estradiol levels is linked to increased metabolic disease risk, prompting investigations into estradiol's impact on metabolic homeostasis.
Estradiol replacement in ovariectomized rodents reverses metabolic impairments, preserving insulin sensitivity and mitigating adipose inflammation.
Research suggests ERα polymorphisms impact metabolic profiles, with tissue-specific transcriptomics shedding light on downstream effects.