[Changes in blood insulin level induced by intravenous or oral glucose in various types of diabetes mellitus].
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Biomedical subjects
Publications and source records attributed to A Orsetti.
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We aimed at investigating relationships between zinc status, blood rheology and blood glucose during exercise. Twenty-one professional football players underwent a triangular maximal exercise test on cycloergometer, with progressively increasing work loads until VO2max. On the whole these subjects had a low serum zinc because nine of them had a hypozincemia (0.54 +/- 0.01 mg/l) which suggested a zinc deficiency. Subjects with low serum zinc were able to perform a lower power output (123 +/- 8.71 vs. 166.27 +/- 14.84 watts, p = 0.029) and exhibited a higher increase in blood lactate during exercise (7.51 +/- 0.81 vs. 5.57 +/- 0.33 mmol/l, p = 0.024) resulting in a lower 2 mmol lactate threshold (44.7 +/- 3.9% vs. 58.9 +/- 4.8% of maximal power output, p = 0.04). They were less able to maintain their plasma glucose and exhibited a tendency towards hypoglycemia (p = 0.0153). Hypozincemia was associated with a higher viscometric RBC rigidity index (p = 0.0009), and this index was negatively correlated to serum zinc (r = -0.68, p = 0.7 x 10(-3)). Blood viscosity at high shear rate (MT90 viscosimeter) corrected for hematocrit (45%) remained higher during exercise in these hypozincemic subjects (p = 0.003). This study suggests that zinc status may influence blood rheology during exercise, either by its direct action on RBC flexibility (demonstrated in vitro) or by its effect on lactate accumulation which may in turn modify erythrocyte fexibility.
Microalbuminuria is not only a predictor of diabetic nephropathy in type 1 diabetes, but also a potent marker of cardiovascular risk, especially in type 2 diabetes. Microalbuminuria also predicts cardiovascular morbidity in the general population. We describe semi-quantitative and quantitative methods for determination of low urinary excretion of albumin. Pathogenetic hypotheses common to both renal and endothelial dysfunction are discussed, suggesting that microalbuminuria may be a link between micro- and macroangiopathy. Improved glycemic control and antihypertensive treatment postpone and potentially prevent development of nephropathy in diabetic patients with microalbuminuria. These interventions must be instituted early in the development of diabetic nephropathy. In type 2 diabetes, prospective studies are needed to evaluate the precise impact of such a therapy on the cardiovascular risk.