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Biomedical subjects

G Crepaldi

Publications and source records attributed to G Crepaldi.

At least 217 records · Page 12Linked to original sources

Short-term and long-term clinical evaluation of a non-amphetaminic anorexiant (mazindol) in the treatment of obesity.

The effectiveness and tolerance of a non-amphetaminic anorexiant drug has been evaluated in a short-term and in a long-term clinical trial in simple obesity and in refractory obesity. In the short-term 'crossover' trial, a more evident effectiveness and tolerance result when the anorexiant is given in a late phase of treatment. The association of an anorexiant drug with the hypocaloric diet was seen to be effective in the treatment of so-called refractory obesity. In the evaluation of the long-term treatment it is seen that weight loss is greater and remains so farr longer periods in patients receiving anorexiant, as compared to controls. This is related to a better maintenance of a restricted calorie regimen. Mazindol did not affect the improvement of glucose tolerance and insulin secretion which follows the weight reduction.

Adolescent↗

Hormonal counterregulation in ethanol-induced hypoglycemia-Glucagon and cortisol secretion in pigs.

Plasma glucagon and cortisol levels were determined in pigs during ethanol-induced hypoglycemia. This hypoglycemia is due to an inhibition of gluconeogenesis which could be related to an abnormal secretion of gluconeogenetic hormones. In six pigs the infusion of ethanol for seven hours (6 mg/kg/min) induced a significant decrease of plasma glucose which was associated with a significant increase of plasma glucagon in the portal vein, femoral artery and hepatic vein. Corresponding with the period of maximal hypoglycemia, plasma cortisol in the femoral artery was also significantly increased. On the other hand, plasma insulin levels were consistently reduced during hypoglycemia. In a second group of six pigs ethanol was infused along with a glucose infusion (3 mg/kg/min) in order to obtain a relatively constant glucose concentration. In this group ethanol did not produce any significant modification of plasma glucagon and cortisol. Therefore, glucagon and cortisol hypersecretion is related to hypoglycemia induced by ethanol. Both the increase in plasma glucagon and cortisol and the decrease in plasma insulin could represent a protective mechanism against alcohol-hypoglycemia.

Animals↗

Tryptophan metabolism "via" nicotimic acid in patients with scleroderma.

The tryptophan metabolism "via" kynurenine was studied in five patients with scleroderma after aminoacid loading. Four of these patients had abnormal tryptophan metabolism, characterized by a large urinary excretion of kynurenine and kynurenic acid in two cases, of kynurenine, 3-hydroxykynurenine and kynurenic acid in one case and of 3-hydroxyanthranilic acid in another case and generally a reduced excretion of xanthurenic acid and its 8-methyl ether in comparison with a group of healthy controls. Only two of the four patients had a normal response to tryptophan loading after pyridoxine administration, while no one of these responded to nicotinamide supplementation. But the simultaneous administration of pyridoxine and nicotinamide to three of these patients normalized the excretory picture after tryptophan loading. This suggested the presence of a combined vitamin deficiency in seleroderma. As four out of five patients showed total excretory values of kynurenine, kynurenic acid and acetylkynurenine higher than that of the controls, the sum of these values might be considered as a characteristic index of scleroderma.

Adult↗

Glucagon secretion in primary endogenous hypertriglyceridemia before and after clofibrate treatment.

Arginine-induced insulin and glucagon secretion preceding and following clofibrate treatment was studied in 13 patients with endogenous hypertriglyceridemia. A positive correlation was demonstrated between fasting insulin and triglyceride levels and between the fasting insulin/glucagon molar ratio and triglyceride levels. In patients with endogenous hypertriglyceridemia, anginine infusion induced a significantly increased glucagon response with respect to that found in controls. No correlation was found to exist between glucagon and free fatty acids (FFA) or between glucagon and triglyceride levels. The same lack of correlation was found in normal subjects rendered hypertriglyceridemic by means of Intralipid infusion, which did not modify the fasting glucagon-like immunoreactivity (GLI) or the GLI response to arginine. Clofibrate treatment induces a triglyceride reduction (incrementTG) which is correlated with the reduction in the insulin/glucagon molar ration (incrementI/G). After clofibrate treatment there is also a significant reduction in fasting GLI levels and in the insulin response to arginine, and an increase in the glucagon response. Clofibrate could exercise its hypolipidemic effect by modifying the relationship between insulin and glucagon levels.

Adult↗

The influence of plasma triglycerides on human growth hormone response to arginine and insulin: a study in hyperlipemics and normal subjects.

Human growth hormone (HGH) response to arginine (25 gm IV in 30 min) and to insulin (0.1 U/kg B.W.) was studied in 12 male patients (mean age 36 +/- 2 years), with normal glucose tolerance and normal body weight, affected with Fredrickson's Type IV primary hyperlipemia. The patients were examined both when plasma triglycerides (TG) were elevated and following clofibrate (2 gm/die for 30-60 days) induced TG reduction. No variations in glucose or FFA behaviour or in body weight were observed after clofibrate. HGH response to arginine was absent, while that to insulin was only inhibited, when plasma TG were elevated. A significant increase in HGH peaks after arginine (from 1.99 +/- 0.59 to 9.34 +/- 1.58 ng/ml) and a slight increment in HGH peaks after insulin (from 23.09 +/- 7.19 to 31.46 +/- 7.95 ng/ml) were observed following reduction in plasma TG. Arginine test was carried out in 7 normal subjects during saline infusion and at the 3rd hour of lipid infusion (Intralipid 20%). HGH response to arginine was absent in all of the subjects during lipid infusion. The HGH response to insulin test, carried out in 9 other normal subjects during saline infusion and at the 3rd hour of lipid infusion (Lipiphysan 15%) was significantly inhibited during lipid infusion. Since lipid infusion provoked an increment, not only in plasma TG but also in FFA, the inhibition of HGH release could be correlated with the elevated plasma levels of both TG and FFA. The results obtained in both spontaneous and experimental hyperlipemia not only confirm the role played by FFA in the regulation of HGH secretion, but also support the hypothesis that elevated TG levels could inhibit HGH response to some stimuli.

Adult↗

Human growth hormone and cortisol response to insulin stimulation in aging.

The influence of age on plasma growth hormone (HGH) and cortisol response to i.v. insulin (0.1 U/kg of body weight) was evaluated in 32 healthy subjects whose ages ranged between 20 and 84 years. A significant reduction in HGH response to insulin was observed with aging. In the young (20-34 years), middel-aged (35-49 years), and elderly (53-84 years) groups, average HGH peaks were 46.51 +/- 7.37, 29.95 +/- 5.35, and 14.31 +/- 2.39 ng/ml while average HGH areas were 2.911 +/- 0.484, 1.654 +/- 0.316, and 0.699 +/- 0.149 mug-min, respectively. Since insulin's hypoglycemic effect became less rapid with aging, this could, in part, explain the progressive decline in the HGH response to insulin. This phenomen may also be attributed to histological changes occurring in the pituitary with aging. Moreover, cortisol response was similar to all three age groups. These findings suggest that, while HGH response to insulin is correlated with age, adrenal response does not show any important modifications with aging.

Adult↗

[Long term treatment of familial hypercholesterolemia with Colestipol, a new anionic exchange resin (author's transl)].

Results relative to long term treatment with Colestipol (a new resin sequestering bile acids) in 23 subjects with familial hypercholesterolemia, 12 with Type II A, 8 with Type II B and 3 homozygotes are reported. The patients had previously undergone treatment with clofibrate together with a hypocholesterolemic diet. After six weeks with placebo, the patients were given 15 g/die active drug for a period of 12 months and a double dose (30 g/die) for a successive period of 4 months. During the experimental trial the same hypocholesterolemic, isocaloric diet which had been followed during the previous hypolipidemic treatment was maintained. In the entire group taken as a whole, the total mean decrease was --56,9 +/- 15 mg/dl (P less than 0,01) after 12 months of 15 g/die Colestipol and --62,8 +/- 13 mg/dl (P less than 0,01) during the following 4 months with 30 g/die Colestipol. The difference between the two periods of treatment (15 g and 30 g/die) is not statistically significant. During the active drug treatment a slight but not statistically significant triglyceride increase was observed. The increase was most marked in the Type II B patients: the triglyceride variations in this group could be partly caused by slight variations in mean body weight. Starting from a mean basal value of 3,9 +/- 0,2 mg/dl, serum uric acid showed a significant increase which was maintained throughout the entire period of treatment, reaching a peak of 5,6 +/- 0,3 mg/dl (P less than 0,001) at the twelfth month. During the experimental trial no significant modifications were observed in the hematological routine analysis and liver functional tests, no malabsorption syndrome and no signs of toxicity were seen. Most frequent side effects were constipation, nausea, metheorism which, with the exception of four cases, which were withdrawn from the study, were reported as being transitory and mild. In conclusion, since Colestipol treatment significantly lowers cholesterol levels in patients with familial hypercholesterolemia and does not manifest any toxicity or serious side effects, it can be used effectively in the long term treatment of this disease which is characterized by an elevated frequency of cardiovascular complications.

Adult↗

Relationship between tryptophan metabolism and vitamin B6 and nicotinamide in aged subjects.

The urinary excretion of tryptophan metabolites was studied in 20 aged subjects (over 70 years) after oral tryptophan loading (100 mg/kg body weight). All the subjects considered showed an abnormal excretion of metabolites with mean values of 24.67% in men and 25.83% in women in comparison to 6.77% in young controls. Among the metabolites the highest excretion was from kynurenine; moreover kynurenic acid and N-alpha-acetylkynurenine were also excreted in signficantly high amounts. The other metabolites too showed increased values. As the abnormal tryptophan metabolism in aging seemed to be in connection with vitamin B6 and nicotinamide, in a group of 7 aged sugjects the urinary excretion of tryptophan metabolites was studied after aminoacid loading with or without simultaneous administration of these two vitamins. The results show that the abnormal excretory pattern is normalized after vitamin administration (from 16.49% to 7.42% total mean metabolite values).

Adult↗