Alterazioni endocrine e metaboliche della donna diabetica in menopausa.

Hormonal and metabolic disorders in menopause play a key role in hyperinsulinemia, insulin resistance and visceral obesity, contributing to dyslipidemia, oxidative stress, inflammation, clotting and atherosclerosis. These conditions all constitute risk factors for cardiovascular disease. In menopausal women estrogen deficiency and the relative hyperandrogenism promote metabolic dysfunction, predisposing to obesity, metabolic syndrome and type 2 diabetes. This review focuses on the role of estradiol (E2) and its receptors (ERs) in the control of energy homeostasis and glucose metabolism. E2 in the hypothalamic nuclei separately controls food intake, energy expenditure and fat distribution. In skeletal muscle, liver, adipose tissue and immune cells, E2 is involved in insulin sensitivity and prevents obesity and inflammation. E2 regulates insulin secretion in pancreatic β-cells. In menopausal women with pre-existing Type 1 and Type 2 diabetes mellitus, climacteric symptoms, metabolic disorders and diabetic complicationsare more severe. Hormone therapy (HRT) is not recommended for the prevention of metabolic disorders in menopausal women, but can be considered part of a tailored global strategy to improve the perception of menopausal symptoms and prevent diabetes complications. For the future, new selective estrogen receptor modulators - SERMs - are undergoing testing; they act only on ERs involved in energy balance and glucose homeostasis which activate cellular pathways, with beneficial metabolic effects by blocking ERs in the breast and uterus. New synthesis peptides (GLP-1 + E2) can transport E2 directly to pancreatic β-cells.