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Biomedical subjects

A V Greco

Publications and source records attributed to A V Greco.

At least 199 records · Page 11Linked to original sources
PubMed1980

[Serum biliary acids in hepatic cirrhosis].

Radioimmunological measurement of serum bile acids has shown that they increase in alcoholic cirrhosis of the liver. In normal subjects, the fasting value of serum bile acids averaged 2.5 +/- 0.41 microM/l, whereas in cirrhotics it was 37.8 +/- 7.9 microM/l (p < 0.001). This technique has proved more specific than routine liver function tests. Measurement of fasting serum bile acids is a sensitive, specific, reproducible index of liver bile function. A quality investigation of primary and secondary bile acids requires the adoption of more sensitive techniques which are not, however, readily adaptable to routine use.

Adult↗
PubMed1980

Reversed-phase high-performance liquid chromatographic separation and quantification of individual human bile acids.

The reversed-phase high-performance liquid chromatographic separation and quantification of individual bile acids is described. Taurine- and glycine-conjugated bile acids were separated and detected directly by an ultraviolet absorbance detector operating at 200 nm. Simultaneous quantitation of at least 100 ng of each conjugated bile acid is possible. Carboxylic (free and glycine-conjugated) bile acids were esterified with p-bromophenacyl-bromide. The reaction, using N,N-diisopropylethylamine as catalyst, yields quantitatively the strongly absorbing p-bromophenacyl esters whch can be determined by absorbance measurement at 254 nm. Simultaneous quantitation of less than 20 ng of each bile acid is possible. The present method is applied to the quantitation of individual bile acids in ten human gallbladder bile samples.

Acetophenones↗
PubMed1980

[Bile lipid composition in subjects with blood lipid disorders (types II and IV). Effect of a new hypolipemic drug (Etofibrate)].

The biliary lithogenous index before and after treatment with Etofibrate, a new hypolipaemizing substance, has been assessed in dyslipidaemic subjects (ypes II and IV). Etofibrate is the result of the association of a molecule of clofibrate and one of nicotinic acid. An analysis of relative molar concentrations of biliary lipides showed that subjects with type IV and IIb dyslipidaemia produced lithogenous bile in base condition, unlike subjects with type IIa dyslipidaemia. After 28 days of treatment with Etofibrate (900 mg/die) a clear-cut increase was observed in the biliary lithogenous index in all types of dyslipidaemia examined.

Adult↗
PubMed1980

Lipid synthesis from the liver in patients with psoriasis.

In psoriatic patients with hyperlipidemia we studied the hepatic lipid synthesis from (1-(14)C)-acetate in human liver biopsy specimens in vitro by a thin-layer radio-chromatography. In psoriatics type IV (according to Fredrickson) a significant increase in (1-(14)C)-acetate hepatic incorporation especially into phospholipids (25%) and triglycerides (52%) was observed; in type IIb increased lipogenesis was phospholipids (24.5%), free cholesterol (44.4%) and triglycerides (29%). Abnormal lipid metabolism often coexists with glucose intolerance in psoriasis; no correlation between hyperinsulinemia and augmented (1-(14)C)-acetate incorporation into hepatic triglycerides was found.

Adult↗
PubMed1980

Insulin resistance in liver cirrhosis: decreased insulin binding to circulating monocytes.

Hyperinsulinemia and insulin resistance have been reported in patients with liver cirrhosis. Since insulin receptor decrease has been demonstrated in some conditions of insulin resistance, we have studied insulin binding to circulating monocytes in eleven patients with alcoholic liver cirrhosis. Specific insulin binding at tracer concentration was lower in cirrhotics than in control subjects (p < 0.005). Insulin binding to monocytes was correlated with basal plasma insulin level in cirrhotics (r = -0.76; p < 0.01). The inhibiting effect of native insulin on 125I-insulin binding was similar in cirrhotics and controls suggesting that concentration rather than affinity of the binding sites is affected in cirrhosis of the liver. These findings suggest that decrease in insulin receptor concentration exists in liver cirrhosis, probably as a consequence of chronic hyperinsulinemia.

Adult↗
PubMed1980

Fetal origin of amniotic fluid insulin in the human mother.

To investigate the origin of insulin in amniotic fluid amniocenteses were carried out in pregnancies with live, dead and anencephalic fetuses. Amniotic fluid insulin of pregnant women bearing live fetuses was 9.0 +/- 2.1 microU/ml; in six women with dead foetuses amniotic fluid insulin was not detected. A significant positive correlation was observed between gestational age and the amniotic fluid concentration of insulin. In the amniotic fluid of the four women bearing anencephalic fetuses, the amount of hormone was within normal limits (10.0 +/- 1.4 microU/ml). Intravenous glucose administration (0.33 g/kg body weight) to the mother doses not influence levels of insulin in amniotic fluid, but brought about changes in amniotic fluid glucose concentration. These findings support the conclusion that human amniotic fluid insulin is of fetal rather than maternal origin.

Adult↗
PubMed1980

Differences in insulin receptors between men and menstruating women and influence of sex hormones on insulin binding during the menstrual cycle.

Specific binding of [125I]insulin to circulating monocytes and erythrocytes from nine normal menstruating women and nine normal men was determined during a 28-day period (one sample every 7 days). In women, insulin binding was higher to both monocytes (P less than 0.001) and erythrocytes (P less than 0.02) in the follicular phase than in the luteal phase. In men, insulin binding to monocytes was similar to the follicular phase values for women; however, insulin binding to erythrocytes from men showed higher values than insulin binding to erythrocytes from women in both the follicular (P less than 0.001) and luteal (P less than 0.001) phases. These differences were due primarily to changes in receptor concentration rather than receptor affinity. An inverse relationship was found between insulin binding to monocytes and levels of 17 beta-estradiol, progesterone, and 17 alpha-hydroxyprogesterone; this relationship was not observed in insulin binding to erythrocytes. The present data, therefore, suggest that sex hormones may play a role in the control of insulin receptors. Furthermore, it appears that other factors exist during the follicular phase that lower insulin binding to erythrocyte insulin receptors. If insulin receptors on circulating cells reflect the behavior of the main insulin target tissues, the present data might in part explain the reduction in glucose tolerance reported by various authors in the second half of the menstrual cycle.

Adult↗
PubMed1980

Effect of dexamethasone and cortisone on insulin receptors in normal human male.

Results of a recent study suggested that depending upon the glucocorticoid or the model used, opposite changes occur in insulin binding; in fact, the increase in insulin receptor number on monocytes after prednisone ingestion in man appears to contrast with previous reports in animals in which a decrease was shown after dexamethasone. To establish whether this apparent discrepancy depends upon the model used in human studies (i.e. monocytes), the effect of dexamethasone and corticone intake on normal men was evaluated. A significant decrease was observed in insulin binding on circulating monocytes 24, 48, and 72 h after both steroids, mainly due to reduced receptor affinity. Furthermore, steroid treatment increased insulinemia which did not appear to be related to insulin binding. These data are in agreement with results in animal studies and appear to suggest that previous data on prednisone do not depend upon the model used (i.e. monocytes) but upon the hormone itself, thus indicating that glucocorticoids, depending upon their chemical structure, may produce opposite changes in membrane insulin binding sites. Furthermore, since dexamethasone and cortisone affect plasma insulin levels in the same fashion as previously reported with prednisone, it is suggested that the variation in insulin binding observed after glucocorticoid treatment is not due to variations in insulinemia.

Cortisone↗
PubMed1979

Effects of insulin on hepatic lipid synthesis in alloxan diabetic rats.

In vitro hepatic synthesis of lipids starting from 1-(14)C-acetate was studied in rats made diabetic by subcutaneous alloxan administration (175 mg/kg b.w.). A second group of diabetic rats was treated with lente insulin. In the alloxan-treated rats, a decrese was observed in hepatic incorporation of 1-(14)C-acetate into phospholipids, triglycerides and esterified cholesterol; there was an increased incorporation into nonesterified fatty acids (NEFA) and free cholesterol. Insulin administration restored lipid synthesis values to normal. On histologic examination, an intranuclear glycogenesis was observed in the hepatocytes of the alloxan-treated rats, along with severe hepatic necrosis; the latter however, only in rats sacrified on the 3rd day. Hepatic steatosis with small, medium and large droplets was present in the insulin-treated rats; signs of cellular degeneration were less evident.

Animals↗
PubMed1979

Glucose, insulin and somatostatin infusion for the determination of insulin resistance in liver cirrhosis.

Twelve patients with liver cirrhosis and ten normal subjects were studied. Using a constant intravneous infusion of glucose, insulin and somatostatin over 2 1/2 hours we determined the stteady state plasma glucose level (SSPG) in order to measure insulin resistance. The results demonstrated that the cirrhotic patients were insulin resistant compared to normals and that plasma glucagon does not account for the insulin resistance in these patients.

Adult↗
PubMed1979

Early insulin and glucagon response to subsequent pulses of arginine, glucose, and tolbutamide in normal man.

To determine the dynamics of insulin and of glucagon secretion in response to several sequential stimuli administered shortly after an arginine pulse (5 g), 20 nonobese, apparently healthy volunteers were given arginine (5 g), glucose (5 g), and tolbutamide (1 g) by rapid intravenous injection. The early insulin and glucagon area 0-8 min was studied. At the intervals and with the dosages used in this study, different stimuli with and without prestimulation with arginine did not lead to changes in early secretion of insulin. There was no exhaustion of the pool of insulin released after multiple sequential pulses. These results suggest a pattern in which stimulation induces a rapid release of insulin and activates the interchange between the stored and labile insulin pool; the 8-min interval is sufficient for the rapid return of the two compartments to a state of equilibrium. Also for glucagon, subsequent different stimuli did not exhaust glucagon release; nevertheless, glucagon is immediately suppressed by a submaximal glucose pulse.

Adolescent↗
PubMed1979

GH secretion in open-angle glaucoma.

Open-angle glaucoma is frequently observed in patients with acromegaly suggesting that the somatotropic hormone might facilitate a condition of glaucoma. The open-angle glaucoma patients studied, displayed higher plasma human growth hormone (HGH) levels than control subjects 60 min (30.3 +/- 1.7 against 16.8 +/- 2.7 ng/ml; p less than 0.001) and 90 min (19.0 +/- 1.9 against 9.3 +/- 1.2 ng/ml; p less than 0.001) after intravenous administration of arginine (25 g in 30 min). The authors support the hypothesis that the increased plasma HGH level may interfere with the regulation of ocular pressure by modifying the flow of aqueous humor from the eyeball via changes in the sclero-corneal trabecular meshwork; these changes are also found in diabetic subjects. The interplay between HGH and changes of carbohydrate metabolism (frequently occurring in glaucomatous patients) may be at the root of the variations of intraocular pressure in open-angle glaucoma.

Arginine↗
PubMed1979

The effect of food intake on insulin receptor in man.

Insulin binding to circulating monocytes was studied in 22 normal volunteers before and 1, 3 and 5 h after a 1400 Kcal meal. Results indicate that 3 h after food intake there is an increase in the specific cell binding fraction (P less than 0.001) with a change in receptor affinity. Data emerging from the present study demonstrate that there are rapid changes in insulin receptor properties during the day. These changes probably play a role in the regulation of the hormonal and metabolic pattern in normal subjects.

Adult↗
PubMed1979

Gastrin response to insulin in patients with cirrhosis of the liver.

Fasting gastrinemia in cirrhotics (48.35 +/- 2.77 pg/ml) was higher than in normal controls (32.93 +/- 0.75 pg/ml; P less than 0.001). After insulin-induced hypoglycemia, the mean increase of gastrin above basal level was 42.29 +/- 1.92 pg/ml in controls and 10.85 +/- 5.05 pg/ml in cirrhosis (P less than 0.001). BAO was 2.53 +/- 0.36 mEq/h in controls and 0.42 +/- 0.004 mEq/h in cirrhotics (P less than 0.001). After i.v. insulin, TAO was 8.42 +/- 0.72 mEq/h in controls and 3.06 +/- 0.26 mEq/h in cirrhotics (P less than 0.001). The authors suggest that the lack of an adequate gastrin and acid response to the hypoglycemic stimulus in cirrhotics might be accounted for by a decreased insulin sensitivity.

Adult↗
PubMed1979

Serum gastrin in portal and peripheral veins after arginine in man.

Immunoreactive serum gastrin from portal and peripheral veins was determined in five controls and in five cirrhotic patients with indwelling portal catheters in basal conditions, during and after 30 min arginine infusion, in order to assess whether the human liver is involved in gastrin metabolism. A significant difference was found between portal and peripheral gastrin concentrations in controls at 0, 60 and 90 min; no significant differences were found in cirrhotics. Our findings support the hypothesis of an at least partial breakdown of endogenous gastrin in the human liver.

Adult↗