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Twelve newly diagnosed and eleven previously unsuccessfully treated diabetics were included in a strictly controlled cross-over trial comparing the efficacy of glipizide with that of a placebo or the previous orally administered antidiabetic drug. All newly diagnosed diabetics responded to glipizide and in eleven of them (91%), the control of the glycaemia was “excellent” or “good”. In the cases with severe diabetes, glipizide achieved on an average a better control of the glycaemia due to meals than that produced by the previous therapy. — Neither hypoglycaemia nor side-effects have been observed. We therefore conclude that glipizide is an effective and safe high potency oral sulphonylurea.

Haematocrit, plasma volume and viscosity were not notably different at rest in fifteen diabetics from those in ten controls. After moderate exercise, plasma volume was reduced and haematocrit was increased significantly more than those in controls. In the diabetic subgroups based on varying degrees of dermal angiopathy, no significant differences were demonstrated. In circulatory steady state during exercise the diabetics responded with a marked increase of systolic blood pressure. The amount of filtrate from the vascular bed to the interstitial tissues was not correlated to increasing systolic pressure. The difference in work intensity between the groups is not of such an order that it can be assumed to influence haematocrit or plasma volume. These findings may indicate increasing permeability of the capillary walls because of changes characteristic of diabetic microangiopathy.

The effects of a new sulfonylurea (Ro 6-4563) have been studied on glucose tolerance, plasma insulin, lipids, and lipoprotein pattern in 29 patients with maturity onset diabetes. After 4 weeks of treatment 3 different reactions have been distinguished and are discussed: I. No response, viz. same glucose tolerance and insulin levels before and after treatment. II. Improved glucose tolerance without increased insulin levels. III. Improved glucose tolerance with higher insulin levels. Sulfonylurea treatment had no effect on plasma lipids or lipoprotein pattern. Clinically “good blood sugar control” could not be correlated with good lipid control. Response II supports the view that sulfonylurea compounds do not necessarily act by increasing plasma insulin levels.

Infrared thermography revealed characteristic abnormalities in the emission patterns over the hands and feet of 16 young diabetics with or without manifest vascular complications. Infrared thermography seems to be a method well suited for further studies of circulation and metabolism in the hands and feet of diabetics.

The rheology of blood cells studied intravascularly, and the relation between blood cells and endothelium was analyzed in vivo by high resolution, vital microscopy in four diabetic patients with varying duration of the disease. In a dipedicled, tubed skin-flap a titanium chamber with optics was implanted. A thin layer of tissue in this chamber was observed microscopically over a period of up to 4 months. Microvascular structure and function were analyzed under normal flow conditions as well as in various test situations with reduced or completely blocked flow in lipaemia and when slight local tissue trauma was added. It was found, contrary to what has hitherto been considered in the literature, that there is no aggregation of blood cells in diabetes, unless the metabolic balance is heavily upset as in acidosis. The rheology of the various types of blood cells is normal even in long-standing diabetes.

The effect of long-term treatment with phenformin and metformin respectively on blood lactate concentrations in relation to submaximal muscular exercise has been examined in 21 maturity-onset diabetics, using a cross-over method. At similar degrees of diabetic control the mean blood lactate concentration during exercise and shortly thereafter was significantly higher when the patients had received phenformin. The mean fasting lactate concentration was 1.07 mmol/l with phenformin and 1.03 mmol/l with metformin and the peak concentration was 2.56 mmol/l and 2.19 mmol/l respectively. The mean fasting blood glucose concentration before the exercise was 11.2 mmol/l with phenformin and 11.3 mmol/l with metformin; the glucose output in the urine during the preceding 24 hours was 93 mmol and 105 mmol respectively. The mean work load during exercise was 60 watts.