[Plasma levels of beta-endorphin in obese subjects with normal glucose tolerance test and in diabetics]. / Livelli plasmatici di beta-endorfina in soggetti obesi normotolleranti e diabetici.

Forty obese subjects with normal glucose tolerance test (NGTT) thirteen diabetic obese subjects and sixteen normal subjects were studied to evaluate the possible interactions between beta-endorphin (B-Ep) and glucose homeostasis. On the basis of baseline B-Ep levels, two subgroups were selected: one group with normal mean values of B-Ep (7.02 +/- 0.59 pmol/l); another group with elevated mean values of B-Ep (18.95 +/- 1.52 pmol/l). No differences between these subgroups were found as regards body mass index (BMI), insulin and glucagon levels. Normal B-Ep values were found in diabetic obese subjects. No significant correlation was found between B-Ep and BMI, insulin or glucagon. Considering that B-Ep is involved in eating behavior and on the basis of our results, we suggest that elevated B-Ep levels can be found only in those obese NGTT subjects whose obesity is probably related to an abnormal modulation of food intake, such as hyperphagia.

Increase in red cell lactate concentration and its reduction by isologous plasma in NIDDM subjects.

We determined red blood cell (RBC) lactate concentrations in NIDDM subjects using an experimental protocol in which diabetic RBCs were incubated over 8 hours both with own plasma and with normal plasma. Furthermore, normal RBCs were incubated both with own plasma and with diabetic plasma. The results indicate that the increased lactate concentrations in RBCs from NIDDM subjects decreased significantly when the same RBCs were incubated in normal plasma. Conversely, lactate concentrations in normal RBCs increased significantly when RBCs were incubated in diabetic plasma. Thus, other than muscle and adipose tissue, RBCs may contribute to increase lactate release for hepatic gluconeogenesis in NIDDM and we suggest that there may be extrinsic plasmatic factor(s) capable of stimulatory effect on diabetic RBC glycolytic pathway.

The effects of muscular exercise on glucose, free fatty acids, alanine and lactate in type I diabetic subjects in relation to metabolic control.

Metabolic effects of muscular exercise were studied in eleven subjects with type I diabetes mellitus during poor metabolic control, and again during good metabolic control, and in ten healthy control subjects. All the subjects were submitted to a submaximal gradual triangular test on an electrically braked bicycle ergometer; glucose, FFA, alanine and lactate were measured at rest, and after exercise. In poorly controlled patients, glucose and FFA were unchanged after exercise, whereas blood alanine and lactate increased by a percentage similar to that of the controls, and well-controlled diabetic patients. Baseline alanine concentrations were lower and lactate concentrations higher than in the controls and well-controlled patients. After adequate metabolic control was achieved, in the well-controlled diabetic patients a normalization of pre-exercise alanine and lactate levels and a decrease in blood glucose and FFA after exercise was observed.

Effects of muscular exercise on erythrocyte adenosine triphosphate concentration in patients with insulin-dependent diabetes mellitus.

Type I diabetes mellitus represents a metabolic disorder in which intracellular glycolytic pathway is inhibited by insulin deficiency, with the subsequent decreased availability of energetic substrates such as ATP. Some aspects of the energetic metabolism in response to an intensive demand (muscular exercise) were investigated, in a group of 10 ketotic diabetic patients, by measuring erythrocyte adenosine triphosphate (ATP) and blood glucose, free fatty acids (FFA) and lactate levels. In the diabetic subjects, in comparison with normal subjects, the decreased levels of erythrocyte ATP at rest did not increase after exercise, while the increased levels of FFA at rest did not diminish after exercise. The results show that the impaired erythrocyte glycolysis may produce reduced levels of ATP not only at rest, but also after exercise, when muscular contraction results in a manifold increase in cellular energy requirements. In addition, other metabolic systems providing energy for the exercising muscle, such as FFA utilization, are impaired in the ketotic diabetic patients.

Effects of dynamic exercise and metabolic control on left ventricular performance in insulin-dependent diabetes mellitus.

In subclinical diabetic cardiomyopathy, previous reports did not positively correlate the altered cardiac performance with metabolic parameters. Fifteen insulin-dependent diabetic subjects, without any clinical or instrumental evidence of heart diseases, were studied. Signs of diabetic microangiopathy were absent. Systolic time intervals, metabolic and hormonal parameters (blood glucose, free fatty acids, blood lactate and plasma norepinephrine) were evaluated at rest and after dynamic exercise during poor (MAGE 6.36 +/- 0.72 mmol/l) and good (MAGE 3.46 +/- 0.66 mmol/l) metabolic control, obtained by means of insulin therapy. Rest values of systolic time intervals were normal during poor and good metabolic control. After exercise, pre-ejection period/left ventricular ejection time ratio increased mainly during poor control as a result of an increased pre-ejection period: conversely, a smaller increase in pre-ejection period/left ventricular ejection time ratio occurred during good metabolic control. The exercise induced free fatty acids utilization did not occur during poor control as it occurred during good control. The percentage of increments in blood lactate was virtually identical in ketotic and non-ketotic patients and in normal subjects. High norepinephrine plasma levels were observed both at rest and during dynamic exercise in poorly controlled diabetic patients. Conclusively, testing of systolic time intervals after exercise might be useful in the detection of preclinical diabetic cardiomyopathy. The decreased cardiac functional reserve observed during poor control might be related to an altered energetic fuel utilization.

Analysis of IgA1 and IgA2 subclass distribution in IgA- containing circulating immune complexes in patients with diabetes mellitus.

Immune complexes (IC) containing IgA1 and IgA2 have been detected in diabetes mellitus. In particular IgA1 and IgA2-IC are equally distributed in type 2 diabetes. On the other hands IgA1-IC are prevailingly found in type 1 diabetes mellitus. IgA2-IC (immune complexes of "mucosal" origin?) seen to be of relevance in the pathogenesis of diabetic microangiopathy.