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Biomedical subjects

G Paolisso

Publications and source records attributed to G Paolisso.

202 records · Page 12Linked to original sources
PubMedDate not supplied

Role of alpha and beta cells in the impaired glucose tolerance of thalassaemic subjects.

Fifty healthy and 12 thalassaemic subjects underwent both an oral glucose tolerance test (OGTT) and arginine test in order to investigate their alpha and beta cell activity. While basal plasma levels were similar in both group of subjects (82 +/- 4 vs 74 +/- 4 mg/dl, p = NS), following glucose intake impaired glucose tolerance was observed in thalassaemic subjects. These subjects showed impaired insulin secretion either in steady-state conditions or after glucose intake. When an arginine test was performed in thalassaemic subjects, impaired insulin secretion with concomitant exaggeration of glucagon response was also observed. In the thalassaemic subjects no statistically significant correlations were found between impaired insulin secretion and iron overload. It is suggested that in thalassaemic subjects beta-cell dysfunction and alpha cell overactivity may lead to the development of diabetes mellitus.

Adolescent↗
PubMedDate not supplied

Glycosylated proteins as an indicator of metabolic control in diabetes: evaluation by aminophenylboronic acid affinity chromatography.

Glycosylated proteins, glycosylated albumin and HbA1 were studied in type I and type II diabetes. Glycosylated proteins were evaluated by a new method: aminophenylboronic acid affinity chromatography. A good correlation was found between total HbA1 and glycosylated proteins in both groups (r = 0.57, p less than 0.05; r = 0.67, p less than 0.01, respectively), but a positive correlation between stable HbA1 and glycosylated proteins was present only in maturity onset diabetics (r = 0.71, p less than 0.01). Glycosylated proteins correlated with glycosylated albumin only in type II diabetes (r = 0.67, p less than 0.01). We hypothesize that in maturity onset diabetes glycosylated proteins and HbA1 reflect a greater glycemic stability while in insulin-dependent diabetes the same proteins reflect a different periodic pattern of glycemic control. Moreover, our data suggest that aminophenylboronic acid affinity chromatography is a suitable tool for routine monitoring of metabolic control in maturity onset diabetes, while further investigations are needed to establish if this method is a useful index of altered glucose metabolism in type I diabetes.

Blood Proteins↗
PubMedDate not supplied

[Magnesium and glucose metabolism].

The interrelationships between magnesium and carbohydrate metabolism have regained considerable interest over the last few years. Insulin secretion requires magnesium: magnesium deficiency results in impaired insulin secretion while magnesium replacement restores insulin secretion. Furthermore, experimental magnesium deficiency reduces the tissues sensitivity to insulin. Subclinical magnesium deficiency is common in diabetes. It results from both insufficient magnesium intakes and increase magnesium losses, particularly in the urine. In type 2, or non-insulin-dependent, diabetes mellitus, magnesium deficiency seems to be associated with insulin resistance. Furthermore, it may participate in the pathogenesis of diabetes complications and may contribute to the increased risk of sudden death associated with diabetes. Some studies suggest that magnesium deficiency may play a role in spontaneous abortion of diabetic women, in fetal malformations and in the pathogenesis of neonatal hypocalcemia of the infants of diabetic mothers. Administration of magnesium salts to patients with type 2 diabetes tend to reduce insulin resistance. Long-term studies are needed before recommending systematic magnesium supplementation to type 2 diabetic patients with subclinical magnesium deficiency.

Animals↗