[Effect of treatment with alkaline bicarbonate mineral water on the metabolic response to physical exercise in insulin-dependent diabetics].
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Biomedical subjects
Publications and source records attributed to M Marcelli.
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A combined abdominoperineal approach is described in which not only coloanal anastomosis but also bowel transection were performed through the anus. It is most suitable for cancer located 4 to 6 cm from the anal verge. The main advantages of the technique are precise lines of bowel transection with desired distal clearance of tumor, and easier and safer mobilization of the distal end of the rectum during the abdominal phase of the procedure.
The response of LH to exogenously administered estrogens was evaluated in a 63-year-old patient affected by complete testicular feminization syndrome (CTFS) with very low testosterone (T) levels, before and after gonadectomy. Prior to gonadectomy a durative fall in gonadotropin levels was observed after estrogen administration, without observing of an estrogenic positive feed-back (EPF) from LH. After gonadectomy, following an initial decrement in both gonadotropins, the characteristic. LH peak was seen, 48 h after E2B (Estradiol Benzoate) administration. This observation, together with the very low T levels that we found in this patient, prompted us to construe that absence of EPF in males is not due, as previously believed, to a direct inhibitory action of T or E2, deriving from T aromatization, on the hypothalamus, but by a still unknown gonadal factor. The hypothesis that this factor has a tubular origin is formulated and discussed.
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The effect of endogenous hyperinsulinaemia, produced by syngeneic transplantation of rat insulinoma at an extrapancreatic site, on pancreatic insulin and pancreatic polypeptide has been examined by radioimmunoassay and immunohistochemistry. Twenty days after subcutaneous transplantation, tumour-bearing rats exhibited marked hyperinsulinaemia and hypoglycaemia, with plasma pancreatic polypeptide concentrations similar to controls. Immunoreactive insulin levels in the head and tail of pancreas of tumour-bearing rats were reduced by 90-95% compared with control animals. Immunoreactive pancreatic polypeptide levels in the head of the pancreas were reduced by 70%, but the relatively low levels of peptide in the pancreatic tail were similar in tumour-bearing and control rats. Insulin and pancreatic polypeptide cells were weakly immunofluorescent in tumour-bearing rat pancreas. In conclusion, the presence of an insulinoma at an extrapancreatic site resulted in a severe depletion of endogenous insulin and pancreatic polypeptide, suggesting that there is a functional relationship between the beta and pancreatic polypeptide cell.
The effectiveness of intrathecal morphine (500 micrograms), intrathecal dermorphine (20 micrograms) and routine intramuscular pentazocine (30 mg) in the relief of postoperative pain, was compared in 150 consecutive patients after elective surgery, in a prospective randomized double blind study. The analgesic effect of intrathecal dermorphine was found to be profound and to last significantly longer (43.41 +/- 1.64 hr) than intrathecal morphine (34.45 +/- 2.35 hr) or the routine pentazocine therapy (10.79 +/- 2.23 hr). The mean postoperative hospital stay in the intrathecal dermorphine (5.6 +/- 4) and morphine groups (6.3 +/- 45) was significantly shorter than in the control group (8.7 +/- 42). Side-effects, as urinary retention, vomiting and headache, were not significantly different in the three groups of patients.
A prospective randomized study was carried out to evaluate the nutritional and clinical results of two reconstructive procedures after total gastrectomy for gastric cancer: Longmire-Mouchet (LM) operation with loop interposition and maintained duodenal transit and Roux-en-Y (RY) reconstruction with duodenal exclusion. 22 patients, 11 with LM reconstruction and 11 with RY reconstruction were studied pre-and postoperatively. The average follow-up was of 30 +/- 8 months. The clinical results were shown to be substantially similar to the two groups. No patients complained of heartburn or dysphagia. At esophagoscopy no signs of esophagitis were detected in both groups. The two time course curves of body weight variation did not show statistically significant differences even though in RY patients the body weight has reverted more rapidly to basal values.
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The effect of chronic administration of tolbutamide (150 mg/kg X day, orally, over 60 days) and glibenclamide (1 mg/kg X day, orally, over 60 days) on pancreatic A, B, and D cell function was investigated in male nondiabetic rats. In a first set of experiments pancreatic hormonal response to metabolic stimuli was evaluated during glucose (11.1 mM) or arginine (10 and 20 mM) infusion in the isolated perfused rat pancreas. The basal levels of insulin (IRI) and glucagon (IRG) were similar in control and in sulfonylurea-treated rats. Tolbutamide treatment markedly depressed the IRI response to glucose (P less than 0.005) or arginine (P less than 0.0005) infusion and the IRG response to arginine (P less than 0.01). After glibenclamide treatment, IRI decreased significantly (P less than 0.0005 and P less than 0.005, respectively) only in response to arginine infusion. This effect was still evident 10 days after the end of treatment. Furthermore, long term glibenclamide administration suppressed somatostatin (SRIF) response to glucose (P less than 0.0005) or arginine (P less than 0.0005). In a different group of rats treated with glibenclamide (1 mg/kg X day, orally, over 60 days) IRI, IRG, and SRIF plasma concentration and blood glucose levels were examined at the end of treatment. The results did not differ significantly from those of a control group. In the same animals, pancreatic IRI, IRG, and SRIF content, measured on acid-ethanol extracts, was reduced (P less than 0.1 vs. controls). These data clearly indicate that long term treatment with sulfonylurea drugs has a suppressive effect on pancreatic endocrine function in rats. The concomitant involvement of A, B, and D cell suggests that this effect is not specific.
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In order to characterize the adrenergic control of the pancreatic A cell the effect on glucagon secretion of three sympathomimetic substances - epinephrine, isoproterenol and phenylephrine - and two adrenergic blocking agents - propranolol and phentolamine - were tested separately in the basal state and during glucagon hypersecretion induced by arginine infusion or glucopenia, using the isolated perfused rat pancreas. Epinephrine and isoproterenol infusion caused a prompt and sustained glucagon release in the basal state and potentiated glucagon response to metabolic stimuli. Insulin secretion was suppressed by epinephrine and slightly stimulated by isoproterenol. The stimulatory effect on glucagon secretion observed during phenylephrine infusion was abolished by concomitant propranolol infusion and potentiated by phentolamine. Insulin secretion was markedly depressed by phenylephrine: this effect was reserved by concomitant phentolamine infusion, while no effect was observed by concomitant propranolol infusion. Propranolol caused a suppression of both glucagon and insulin secretion, while phentolamine slightly enhanced glucagon and insulin production. In conclusion, beta-adrenergic receptor stimulation markedly increased pancreatic glucagon secretion and slightly enhanced pancreatic beta-cell activity; conversely, alpha-adrenergic agents markedly depressed insulin secretion while scarcely influencing glucagon production.
In order to characterize the adrenergic control of pancreatic A cell, the effect on the glucagon secretion of three sympathomimetic substances (epinephrine, isoproterenol, phenylephrine) and two adrenergic blockers (propranolol and phentolamine) have been separately examined by the isolated perfused rat pancreas. The study was performed in basal state and during glucagon hypersecretion induced by arginine or glucopenia. Epinephrine and isoproterenol infusion determined a prompt an sustained glucagon release both in the basal state and during glucagon hypersecretion. The effect of phenylephrine infusion was slight. In the presence of propranolol, glucagon secretion induced by metabolic stimulus was significantly depressed. The glucagon secretion in the same experimental conditions was insignificantly enhanced by phentolamine. Finally propranolol infusion reverse the glucagon secretion induced by phenylephrine. In conclusion the pancreatic glucagon secretion in our model of study is clearly induced by B adrenergic receptor stimulation.
Two groups of receptors, one which develops a stimulating effect (alpha 1), the other an inhibitory effect hae recently been isolated in the alpha adrenergic group. In order to type the B cell adrenergic receptor of the endocrine pancreas, which mediates the inhibitory action exerted by the catecholamines on insulin secretion, the release of this hormone was evaluated in the presence of five alpha simpathomimetic substances that have a decreasing degree of efficiency on the adrenergic alpha 2 receptor of the presynaptic sympathic nerve terminal. The order of potency with which the alpha agonists tested depressed IRI secretion is superimposable on that of their potency on the sympathetic nerve and alpha 2 receptor. We concluded that adrenergic inhibition of insulin secretion is mediated by an alpha 2 receptor.
A new in vitro pancreas-intestine model which makes it possible to study the physiopathology of the intero-insular axis in greater depth, as it eliminates interference from other system, is proposed. The model, which is composed of the rat pancreas, duodenum and the first 25 cm of the small intestine, conserves both the circulation and the in vivo anatomical reltionship intact. Experiments were designed to evaluate the effect of a drug-induced disaccharidase-activity block on insulin secretion. The results obtained confirm the validity of the proposed model in investigating the entero-insular axis.
The antibody reactive in antibody-dependent, cell-mediated cytotoxicity (ADCC) to influenza virus-infected cells was measured in two groups of seven volunteers each, before and after immunization with inactivated or live attenuated A/Victoria/3/75 influenza virus vaccines. Age-matched controls were seven adult individuals who experienced natural influenza infection due to A/Victoria/3/75-like virus strain. After inactivated whole influenza virus immunization all the subjects showed a significant rise of the antibody reactive in ADCC (from a mean value of 4.7% to 17.1% cytotoxicity, before and 5 weeks after immunization, respectively) as well as of hemagglutination inhibition (HI) antibody (fourfold or greater increase). These immune responses were similar to those observed among naturally infected controls. After live attenuated virus vaccination, no significant increase in titer of antibody reactive in ADCC was detected, even though the vaccine induced significant increase of HI antibody titer. Little correlation was found between ADCC and HI antibody rises in sera of recipients of inactivated virus vaccine and of naturally infected individuals while, in live attenuated influenza virus vaccines, the rise of HI antibody titer did not correspond to a significant increase of ADCC antibody titer did not show subjects who developed a significant rise in ADCC antibody titer did not show significant variation in antibody to neuraminidase and/or to complement fixation influenza virus antigens.
The incidence of end-stage renal failure has increased in Italy from 70-80 to 120 per 1x10(6). About 20-30% of patients with diabetes develop nephropathy, usually within 20-25 yrs after disease onset. Diet plays an essential role in the therapy of diabetic nephropathy. A well planned diabetic diet with intensive glycemic control can significantly reduce the risk of microalbuminuria development, and moderate protein restriction reduces hyperfiltration and intraglomerular pressure, and retards the progression of diabetic glomerulopathy. Various studies have shown a positive effect of diet with a protein intake of approximately 0.8 g/kg(-1)/day(-1) in patients with overt nephropathy, with a further restriction to 0.6 g/kg(-1)/day(-1) when the glomerular filtration rate begins to fall. Extra protein intake should counterbalance massive proteinuric losses.
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