I Geronooz’s research while affiliated with University of Liège and other places

Smoking is a major risk factor for cardiovascular disease. It is associated with endothelial dysfunction and lipid disorders similar to those found in the insulin resistance syndrome. Studies have thus tried to demonstrate a relationship between smoking and insulin resistance, and between smoking and type 2 diabetes mellitus. Even if their results may sometimes differ, smoking does seem to be associated with an impaired insulin sensitivity that is proportional to tobacco consumption. Nicotine replacement therapies seem also to generate a certain, though lower, degree of insulin resistance. If there is no major weight gain after smoking cessation, the latter is accompanied by a progressive return to normal insulin sensitivity. Several large epidemiological studies recently demonstrated that smoking could increase the risk of type 2 diabetes mellitus, with a relative risk between 1.5 and 3.0. Finally, among type 2 diabetic patients, smoking has a harmful effect on metabolic control and long-term complications of the disease, at least partially by increasing the components of the insulin resistance syndrome. All these observations represent further argument to promote smoking cessation in the general population, and more particularly in individuals at risk to develop type 2 diabetes, as well as in the diabetic population.

Besides dietary approaches, various pharmacological means have been recently developed in order to better control postprandial hyperglycaemia. This objective may be obtained: 1) by slowing down the intestinal absorption of carbohydrates; 2) by insuring a better insulin priming soon after the meal; and 3) by inhibiting post-prandial glucagon secretion or action. Some hormones (amylin, glucagon-like peptide-1) can slow gastric emptying while alpha-glucosidase inhibitors (acarbose, miglitol) retard intestinal digestion and resorption of complex carbohydrates. A more physiological post-meal profile of insulin may be obtained in type 2 diabetes by using new insulin secretagogues of the glinide family (repaglinide, nateglinide) with an earlier and shorter insulinotropic action or, mainly in type 1 diabetes but also in type 2 diabetes, by using short-acting insulin analogues (lispro. Asp B28) or inhated insulin the action of which is faster than that of subcutaneous insulin. Post-prandial glucagon secretion can be inhibited by amylin. GLP-1 or insulin while other glucagon antagonists are currently in development.

Finapres is a device able to continuously and non invasively measure arterial blood pressure by photoplethysmography in the finger. It can be used in various dynamic tests which involve cardiocirculatory adjustments, as a passive posture test ("tilt test") or an active orthostatic test (from squatting to standing position in the so-called squatting test). It represents a valuable help in the diagnosis of orthostatic hypotension (of endogenous or iatrogenic origin), of autonomic neuropathy (secondary to diabetes mellitus or to a neurological disease) or of vasovagal syncope. All these conditions are characterized by a defect of arterial and venous vasoconstriction and by an insufficient reflex tachycardia because of autonomic dysfunction.

Gestational diabetes, even if it seems to induce far less foetal complications than classical type 1 or type 2 diabetes mellitus, may be deleterious for the child. We will successively consider the complications that could affect the child during gestation, during the neonatal period and during adult life. These consequences for the offspring require optimal screening and management of gestational diabetes mellitus.

Defined as glucose intolerance with onset or first recognition during pregnancy, gestational diabetes mellitus represents in fact an heterogeneous clinical entity which may concern 1 to 4% of all pregnant women in our country. Its adverse effects on the mother and her child, the need for a universal screening and the mode of screening are still controversial. Screening may be made either by a first test with a 50 g oral glucose load (the so-called O'Sullivan test), confirmed if positive by a 100 g oral glucose tolerance test (OGTT), or at first glance by a 75 g OGTT performed between the 24th and 28th weeks of gestation. The treatment of gestational diabetes is based on diet. In case of diet failure to obtain good glucose control, insulin therapy should be proposed.

Pregnancy is associated with important changes in mother metabolism, especially in late gestation, among which a decreased glucose tolerance caused by insulin resistance. In some of these women, glucose intolerance is increased by a defect in B-cell function and diabetes mellitus occurs. These women who develop a gestational diabetes need a close follow-up because they are at high risk for further development of diabetes, especially type 2 diabetes.