Insulin sensitivity decreases for the first time in females at the time of menarche. A much more profound decrease in insulin sensitivity is observed at the end of pregnancy. This physiological insulin resistance is not accompanied by a rise in overall sympathetic activity as reflected in plasma noradrenaline levels, but there is evidence of moderate sympathetic overactivity in muscle and the heart. Pre-eclampsia is characterized by increased insulin resistance, sympathetic overactivity and a particular lipid profile. Thus it is the first manifestation of metabolic syndrome. Women with a history of pre-eclampsia have persistent insulin resistance after pregnancy associated with increased sympathetic activity of the cardiovascular system, and coronary artery disease later in life. Aging is accompanied by a greater increase in sympathetic traffic in women than in men, and inflammation (measured via C-reactive protein) seems to be more strongly related to metabolic syndrome in women than in men. The clinical relevance of these observations remains to be shown. As the key factors of metabolic syndrome, such as insulin resistance and sympathetic overactivity, are closely inter-related, treatment should be aimed at cutting the vicious circle at many points: lifestyle modification (diet, increasing exercise) as a basis of therapy, use of insulin sensitizers (e.g. metformin) to decrease insulin resistance, central sympatholytics (e.g. moxonidine), and AT-receptor blockers or angiotensin-converting enzyme (ACE) inhibitors to overcome sympathetic overactivity, hypertension and inflammation.

Gestational diabetes mellitus (GDM) is defined as glucose intolerance with onset or first recognition during pregnancy. Data from Western countries suggest that the prevalence of GDM is increasing, being almost 10% of pregnancies and probably reflecting the global obesity epidemic. The majority of women with GDM seem to have beta-cell dysfunction that appears on a background of chronic insulin resistance already present before pregnancy. In less than 10% of GDM patients, defects of beta-cell function can be due to autoimmune destruction of pancreatic beta-cells, as in type 1 diabetes, or caused by monogenic mutations, as in several MODY subtypes. Diagnostic criteria for GDM vary worldwide and there are no clear-cut plasma glucose cut-off values for identifying women at a higher risk of developing macrosomia or other fetal complications. Because the oral glucose tolerance test (OGTT) is restricted to high risk individuals, 40% of GDM cases are left undiagnosed. Therefore, in high risk populations almost universal screening is recommended; only women considered to have very low risk do not need screening. Diet and exercise are the key elements in the treatment of GDM. If necessary, either insulin, certain oral hypoglycemic agents or combinations can be used to achieve normoglycemia. After delivery, women with GDM and their offspring have an increased risk for developing the metabolic syndrome and type 2 diabetes. Thus, pregnancy may act as a "stress test", revealing a woman's predisposition to T2D and providing opportunities for focused prevention of important chronic diseases.

Maternal overweight, obesity and consequently the incidence of gestational diabetes are increasing rapidly worldwide. The objective of the study was to assess the efficacy and cost-effectiveness of a combined diet and physical activity intervention implemented before, during and after pregnancy in a primary health care setting for preventing gestational diabetes, later type 2 diabetes and other metabolic consequences.

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The metabolic syndrome consists of a combination of risk factors that include abdominal obesity, atherogenic dyslipidaemia, hypertension and insulin resistance. It increases the risk of cardiovascular disease and type 2 diabetes. The increased risk of cardiovascular disease is higher in women than in men. The first manifestation of metabolic syndrome may occur in pregnancy presenting as gestational diabetes or preeclampsia. Both conditions are associated with increased insulin resistance. Also metabolic syndrome is more common in polycystic ovarian syndrome. It has been suggested that there is a metabolic syndrome resulting from the menopause due to estrogen deficiency, as many of the risk factors are more prevalent in postmenopausal women. Also estrogen replacement improves insulin sensitivity and reduces the risk of diabetes. The key elements in managing the metabolic syndrome are weight reduction, increasing physical activity and diet modification. If blood pressure, lipid and glycaemic control are not achieved through these interventions then pharmacological therapy will be required.