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Biomedical subjects

R Torella

Publications and source records attributed to R Torella.

137 records · Page 8Linked to original sources
PubMedDate not supplied

[Beta-endorphin and obesity. Possible pathogenetic implications].

Several experimental data have documented the ability of both opiates and opioid peptides to stimulate food intake. On the other hand, the plasma beta-endorphin levels found in obese patients are higher than those observed in normal-weight controls, which may have pathogenetic implications. We have investigated the responses of plasma glucose, insulin, C-peptide and glucagon to an infusion of human beta-endorphin in formerly obese subjects who had obtained by dieting the normalization of body weight and in lean controls. The data show that: a) the increased plasma beta-endorphin concentrations found in human obesity are not corrected by normalization of body weight; b) formerly obese subjects behave as obese subjects in their metabolic and hormonal responses to beta-endorphin.

Adult↗
PubMedDate not supplied

Beta-endorphin and islet hormone release in type-2 diabetes mellitus the effects of normoglycemia, enkephalin, naloxone and somatostatin.

The present study was aimed at characterizing the effects of beta-endorphin on plasma glucose, insulin and glucagon plasma levels in subjects with type-2 diabetes mellitus. Infusion of 0.5 mg/h human beta-endorphin produced significant and simultaneous increments in both insulin and glucagon concentrations and decreased plasma glucose levels (-18 +/- 4 mg/dl, 60 min level, p less than 0.01). When the same diabetics were rendered euglycemic by an insulin infusion (1 mU/kg/min), beta-endorphin did not produce the expected decrease in plasma glucose concentrations nor raise plasma insulin levels; only the response of glucagon was preserved. Normal subjects were rendered hyperglycemic by an intravenous glucose infusion to match the plasma glucose levels of diabetic subjects. In this condition, beta-endorphin produced a significant increase of insulin concentrations, whereas glucagon remained suppressed. The intravenous administration of the long-acting met-enkephalin analogue DAMME (0.25 mg) blunted the hormonal responses to the subsequent beta-endorphin infusion in diabetic patients, although the inhibition was short-lived (30-40 min). Naloxone (5 mg), an opiate antagonist, did not produce any significant change in the insulin and glucagon responses to beta-endorphin, while somatostatin (0.25 mg/h) completely abolished the hormonal responses to the opioid.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMedDate not supplied

Studies on the mechanism of salicylate-induced increase of insulin secretion in man.

Salicylate compounds are known to increase basal and stimulated insulin secretion in man. In our studies, infusion of lysine acetylsalicylate (72 mg/min) increased basal insulin levels and amplified insulin responses to glucose (5 g i.v.), arginine (5 g i.v.) and tolbutamide (1 g i.v.). Verapamil, an organic calcium antagonist, did not modify LAS-induced increase of basal insulin levels, but reduced the effect of LAS on glucose-induced insulin secretion. Calcitonin and somatostatin, two agents that inhibit basal and glucose-stimulated insulin secretion, inhibited the insulin response to glucose in presence of LAS infusion. The ability of salicylate compounds to augment insulin secretion might be due to multiple sites of action in the Beta-cells.

Adult↗
PubMedDate not supplied

A preliminary note on inhibiting effect of alpha-tocopherol (vit. E) on protein glycation.

Human plasma albumin was incubated in 25 mM/l glucose at 37 degrees C for up to sevent days. Aliquots of this mixture were also incubated with alpha-tocopherol (Vitamin E) at 2 mg/dl, 4 mg/dl and 8 mg/dl, respectively. Vitamin E inhibited protein glycation and, furthermore, shows a dose-dependent effect. This report suggests the possibility of using Vitamin E, at therapeutic doses, to obtain the inhibition of non-enzymatic glycation.

Blood Glucose↗
PubMedDate not supplied

Thrombocytopenia as a sensitive marker of immunologic activity in a patient with autoimmune chronic active hepatitis.

The case of autoimmune chronic active hepatitis in a 57-year-old female is reported. Onset was signalled by an abrupt and dramatic thrombocytopenia, which was also the only laboratory parameter able to monitor treatment and progression of the disease. It is concluded that thrombocytopenia together with the presence of antiplatelet-antibodies might be useful markers to monitor the treatment and evolution of the disease.

Autoantibodies↗