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G Viberti

Publications and source records attributed to G Viberti.

84 records · Page 5Linked to original sources
PubMed1981

Correction of exercise-induced microalbuminuria in insulin-dependent diabetics after 3 weeks of subcutaneous insulin infusion.

The effect of metabolic near-normalization, induced by continuous subcutaneous insulin infusion, on the exaggerated microalbuminuria of exercise was studied in eight insulin-dependent diabetic men selected for normal resting albuminuria. Patients were studied in randomized order during the ordinary glycemic control of conventional insulin treatment (CIT) and after 3 wk of "super-control" with continuous subcutaneous insulin infusion (CSII). Seven age-matched healthy men were used as controls. In the diabetics the albuminuric response to fixed-load bicycle exercise (600 kpm/min for 20 min) during CIT greatly exceeded that of the normal controls (P less than 0.01). After 3 wk of optimal plasma glucose control, urinary albumin excretion rates in response to the same exercise load were significantly reduced (P less than 0.02) in the diabetics and became statistically indistinguishable from that of the normal controls. The urinary excretion rate of beta 2-microglobulin, an index of tubular function, was not increased significantly by exercise either during CIT or CSII. The plasma glucose fall after exercise was greater (P greater than 0.001) on CIT (8.5 +/- 0.9 mmol/L) than on CSII (4.0 +/- 0.6 mmol/L). The pulse rate acceleration in response to exercise was significantly reduced after 3 wk of CSII (P less than 0.05). The exercise-induced systolic blood pressure rise was similar in controls and diabetics on both therapeutic regimens. Thus, a period of metabolic near-normalization in the diabetic corrects the abnormal transglomerular passage of albumin induced by moderately strenuous muscular exercise and reduces the exercise tachycardia. Improved control with CSII appears to reduce greatly the risk of exercise-induced hypoglycemia, despite much tighter glycemic control.

Adult↗
PubMed1976

Effect of the antihistaminic agents meclastine and dexchlorpheniramine on the response of human growth hormone to arginine infusion and insulin hypoglycemia.

Histamine is found in most tissues including the central nervous system. Here it reaches the highest concentrations in the hypothalamus and in the median eminence. In order to evaluate the possible role of endogenous histamine in the control of human growth hormone (hGH) secretion, we investigated the effect of two anti-histamine drugs, meclastine and dexchlorpheniramine, on the hGH response to arginine infusion and to insulin hypoglycemia in 30 normal subjects. The oral administration of meclastine for three days or the intravenous infusion of dexchlorpheniramine significantly reduced the hGH response to arginine infusion. Neither drug affected the secretion of hGH following insulin hypoglycemia. These results suggest that histamine is involved in the control of hGH release, at least in response to arginine. Our data are consistent with the finding that histamine stimulates GH release in the baboon (Meyer and Knobil, Endocrinology 80: 163, 1967) and with previous results indicating that the release of hGH in response to different stimuli is subject to different regulatory mechanisms.

Adult↗
PubMedDate not supplied

Inhibitory effect of clofibrate on arginine-induced insulin secretion in chemical diabetes.

Clofibrate 3 g/die for 10 consecutive days, significantly reduced arginine-induced IRI release in chemical diabetics and in normal controls, whether of normal body weight or obese. Blood glucose levels were not affected by clofibrate. In agreement with previous findings, it would appear that clofibrate, administered for short periods does not lead to a decrease in glucose tolerance. However, studies relating to the effect of chronic clofibrate administration in chemical diabetes are needed in order to be sure that prolonged inhibition of IRI secretion does not lead to overt diabetes.

Antigens↗
PubMedDate not supplied

Genesis and evolution of proteinuria in diabetes mellitus.

Approximately 40-45% of insulin-dependent diabetic (IDD) patients will develop, with time, clinical proteinuria, a forerunner of certain renal failure. Before this, however, up to 45% of IDD patients excrete supranormal amounts of protein in the urine, though still undetectable by dipstix test. This microproteinuria appears to be glomerular in origin, consists mainly of albumin and IgG, and is associated with poor glycemic control and marginal elevation of arterial pressure. Glomerular hemodynamic disturbances, and loss of charge selectivity of the glomerular membrane, are probably responsible for this microproteinuria, which appears reversible by correction of hyperglycemia and raised blood pressure. Once the dipstix test becomes positive (i.e. total urinary protein excretion exceeds 0.5 g/24h) and blood pressure rises into the hypertensive range, glomerular filtration rate (GFR) falls relentlessly. By the time GFR is as low as 20 ml/min/1.73 m2, more IgG relative to albumin is being filtered, giving rise to a low selectivity proteinuria, a condition consistent with changes in the size selectivity properties of the glomerular filtre. Glycemic control does not affect the decline in GFR, although blood pressure control and low protein diet can slow it, presumably by altering the self-perpetuating hemodynamic disturbances that occur in surviving glomeruli. The recent demonstration that IDD patients with microalbuminuria in excess of 30 micrograms/min have approximately a 20-fold increase in risk of developing persistent detectable proteinuria has provided a link between these two phases of diabetic nephropathy. The reversibility of the early microalbuminuria heralds a real chance of preventing the later irreversible phase of end-stage renal failure.

Blood Glucose↗
PubMedDate not supplied

Etiology and prognostic significance of albuminuria in diabetes.

Persistent clinical proteinuria (i.e., urinary protein excretion greater than 0.5 g/24 h) is an ominous development in a person with diabetes. It eventually leads to a decline in the glomerular filtration rate and ultimately to end-stage renal failure or premature cardiovascular mortality. Progression of renal disease appears to be related to arterial blood pressure and protein intake and is primarily independent of the metabolic state. More sensitive immunoassays for detecting low concentrations of albumin in urine have led to recognition of subclinical increases in albumin excretion rates in nonclinically proteinuric diabetic patients, a phenomenon named microalbuminuria. Studies have shown that patients with microalbuminuria have a significantly increased risk for clinical proteinuria and cardiovascular mortality. Microalbuminuria is rarely found during the first 5 yr of a patient's diabetes, suggesting that it is a sign of early glomerular damage rather than a marker for susceptibility to it. In patients with non-insulin-dependent diabetes mellitus (NIDDM), an association has been found between microalbuminuria and coronary heart disease, but this relationship needs further investigation. In patients with insulin-dependent diabetes mellitus (IDDM), this subclinical form of proteinuria is associated with poor metabolic control and, more important, with marginal elevation of blood pressure. Correction of hyperglycemia by intensified insulin treatment might arrest progression to persistent clinical proteinuria; moreover, restricted protein intake and lowering of blood pressure have been shown to reduce the albumin excretion rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Albuminuria↗
PubMedDate not supplied

Recent advances in understanding mechanisms and natural history of diabetic renal disease.

A large subset of individuals with insulin-dependent diabetes mellitus (IDDM) develops clinical nephropathy that progresses to end-stage renal failure. Identification of clinically proteinuric patients has limited impact on management of the condition. No treatment strategy has succeeded in permanently arresting the evolution of clinical nephropathy. However, important advances have been made in slowing its progress, and these are reviewed in this study. Treatment of raised blood pressure early in the course of diabetic renal disease has emerged as the most effective therapeutic measure. Susceptible individuals can be detected before persistent proteinuria becomes manifest by screening IDDM patients for microalbuminuria, which has proved predictive of persistent proteinuria in approximately 80% of cases. Microalbuminuria can be associated with a raised glomerular filtration rate and is often accompanied by subclinical increases in arterial blood pressure. The independent predictive significance of the two latter variables remains to be established in humans. Unfortunately, microalbuminuria is not apparent until 5 yr after stabilization of newly diagnosed diabetes, suggesting that it is a marker of early disease rather than an indicator of susceptibility. However, many therapeutic interventions, ranging from blood glucose control to low-protein diet and angiotensin-converting enzyme inhibition, are effective in reducing or even normalizing microalbuminuria. If current controlled trials show that treatment of microalbuminuric patients prevents progression to clinical nephropathy, the diagnostic criteria for diabetic renal disease will require radical revision.

Albuminuria↗