Primary research

Low Estrogen Exposure and/or Defective Estrogen Signaling Induces Disturbances in Glucose Uptake and Energy Expenditure

Estradiol and its receptors are key players in the physiology and insulin production capacity of the β cells of pancreatic islets. Estradiol administration is associated with pancreatic islet hypertrophy and increased insulin release from the β cells in rats. Islet cells isolated from ovariectomized mice respond to glucose with a smaller insulin release than islet cells from intact mice.

After menopause, estrogen loss decreases the insulin secretion, which is transitorily compensated by its reduced elimination. An estrogen deficient milieu endangers the balanced glucose uptake and energy expenditure of skeletal muscles leading to insulin resistance.

Postmenopausal women never using HRT are obviously insulin resistant and exhibit increasing inclination to the associated comorbidities. With ageing, every year after menopause is associated with continuous estrogen loss and parallel advancing insulin resistance.

For women aged 55-65 years, weight gain and obesity are their major health risks. In postmenopausal women, deepening dysmetabolism, obesity and disturbance of male to female sexual steroid levels are associated with increased prevalence of metabolic syndrome, type 2 diabetes, cardiovascular disease and malignancies.