In postmenopausal women, partly in relation to advancing age and partly due to oestrogen deficiency, there is a frequent increase in body weight, and more specifically, in android fat distribution. In addition, loss of ovarian function is associated with the development of a more atherogenic profile with increased triglycerides, LDL-cholesterol and its smaller dense subfractions, decreased HDL- and HDL2-cholesterol and, potentially, an irregular increase in Lp(a). Not only does oestrogen therapy counteract all these changes towards a definitely less atherogenic profile but oestrogens seem also implicated in reducing LDL oxidative products, in favouring a higher ratio of prostacyclin to thromboxane and, potentially, of endothelium derived relaxing factor to endothelin, and also in acting as a calcium antagonist in the vessel wall. All of these favourable vascular effects are not solely attributable to lipid-related oestrogen effects. Excess weight and central obesity, diet changes and lack of exercise, more frequent with advancing age, all concur to alter glucose tolerance and increase insulin resistance during the postmenopause. Impaired glucose tolerance and diabetes mellitus may be found in nearly 20% of women aged 55 to 65 years. In addition, oestrogen deficiency may be further responsible for decreased pancreatic insulin secretion and alteration of its metabolic clearance rate-changes that can be reversed toward improved insulin secretion and sensitivity by oestrogen treatment in small dosages. By contrast, synthetic androgenic progestins can counteract these effects of oestrogens more than progesterone derivatives do, and they may partly help to promote insulin resistance and hyperinsulinism.(ABSTRACT TRUNCATED AT 250 WORDS)