Insulin and glucagon concentrations in portal and peripheral veins in patients with hepatic cirrhosis.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to L Altomonte.
Explore the source record for details and available documents.
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.
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.
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.
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.
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.
Many factors are to be considered in maintaining normal blood pressure. Authors study the behavior of urinary kallikrein (U.K.) and plasma dopamine-beta-hydroxylase (DBH) activity in various forms of hypertension. The values of U.K. excretion in normals were 20.5 +/- 1.8 E.U./24 h. In essential hypertensive patients (9.4 +/- 2.0 E.U./24 h) U.K. decreased, while in secondary hypertension it was significantly higher (33.8 +/- 3.0 E.U./24 h). Plasma DBH activity in essential hypertensive patients (17.72 +/- 2.33 I.U./ml) was similar to controls (20.22 +/- 1.39 I.U./ml); in secondary hypertension the mean values of plasma DBH were decreased (12.31 +/- 2.55 I.U./ml). No correlation between U.K. and plasma DBH activity was observed in normals and in various forms of hypertensive patients. U.K. seems a more reliable factor than plasma DBH in defining the different types of hypertension.
Cirrhotics presented higher insulin production, in the presence of a drop in glycaemia significantly less than controls, following 1 g of tolbutamide i.v. The drug also brought on a rapid drop in NEFA and a rise in plasma growth hormone. The pathogenesis of altered glucose tolerance in liver cirrhosis is discussed.
Decreased increases in blood sugar by comparison with control subjects was noted in patients with cirrhosis of the liver after i.v. administration of 1 mg glucagon. Insulin secretion was similar to that observed in the controls. Basal GH values were higher in the liver patients, whereas after glucagon they displayed a gradual and progressive increase with a peak at 60'. No significant differences in GH pattern were noted in the two groups, however.
A 500 mg L-Dopa administration in normal and cirrhotic subjects does not determinate a significant varation of plasma glucose and insulin level, while a peak plasma GH level in both cirrhotic and normal subjects occurred at 90' with a significantly greates values in cirrhotics. It is doubtful to affirm that a high plasma GH level is the only one factor which responsable of glucose intolerance in cirrhotic subjects, when there are many others factors contribute to it in synergic way. In order to elucidate the hypothesis on possible pathogenetic mechanism it is discussed some of our own experience and observations.
Recently it has been studied a possible pathogenetic role of GH in diabetic angiopathy. The purpose of the present study was to verify whether the diabetic retinopathy is associated or not with a high plasma GH level. In an attempt to answer this question we did the dosage of plasma GH after a oral glucose load (110 g), Insulin (0,1 U/Kg) i.v., and arginin i.v. (25 g/30'). The plasma GH measurements were approximately the same as in normal patients. The Authors underline the importance of GH in pathophysiology of diabetic angiopathy and report all recent literature on this argument.
Blood sugar, insulin and GH values were examined in two groups of cirrhosis of the liver patients, with and without ascites, after the administration of 100 g glucose per os. No significant differences between the two groups were observed. Insulin values were higher than those in the controls, with a pattern similar to that noted in subjects with chemical diabetes. GH values were higher than in normal subjects and secretion was not suppressed.
Explore the source record for details and available documents.
Measurements of urinary kallikrein using an esterolytic assay revealed higher levels in patients with liver cirrhosis than in a control population. The range of excretion in 33 patients with cirrhosis was from 18.68 to 85.20 E.U. per 24 hours with a mean excretion of 39.42 plus or minus 2.84 E.U. Kallikrein excretion in the control group ranged from 13.20 to 39.50 E.U. per 24 hours with a mean of 24.44 plus or minus 1.66 E.U.
The present study was performed in order to evaluate the plasma glucose pattern in cirrhotic patients who, in the course of a continuous somatostatin infusion (500 microgram/h), were given pulses of glucagon (1 mg i.v.). In normal as well as in cirrhotic subjects somatostatin infusion provoked a marked reduction of the IRI plasma level and this was uninfluenced by subsequent glucagon administration. The rise in plasma glucose level in response to i.v. glucagon administration during somatostatin infusion was less marked in cirrhotics compared to normal subjects. This can be attributed to a variety of factors such as reduced number of liver cells or quantitative or qualitative changes of the liver cell glucagon receptors. Glucagon does not seem to contribute to the pathogenesis of carbohydrate intolerance in liver cirrhosis.
eleven male cirrhotic subjects, all with impaired glucose tolerance (IGT), were studied. Insulin binding to circulating erythrocytes was evaluated. The specific bound fraction was decreased compared to normals (5.95 +/-0.76 vs 7.08 +/- 0.84%; p less than 0.005). An negative correlation was found between fasting insulin and bound fraction (r = -0.68; p less than 0.05). We suggest that serum insulin may be chronically augmented as a consequence of liver damage. This induces a down-regulation of insulin receptors that is responsible for insulin resistance and at least in part for the impairment of glucose tolerance.
A correlation between increased platelet adhesiveness and aggregation and the development of angiopathy in diabetes mellitus can be made. Thromboxane produced by platelets represents a potent platelet aggregation factor. We studied the platelet TXB2 production during blood coagulation in carefully selected patients with type II diabetes mellitus in good metabolic control and the results were correlated with the presence or absence of microangiopathy, fasting blood glucose levels, type of therapy, age, duration of diabetes and the most important hematochemical parameters. No statistically significant differences were found between serum TXB2 concentrations in diabetic patients and control subjects, in diabetics with or without microangiopathy and in diabetics on insulin therapy or on oral hypoglycemic agents. We did not observe any correlation between TXB2 production and age, duration of diabetes, sex, basal blood glucose levels, total and HDL-cholesterol, triglycerides, blood creatinine and blood electrolytes. The thromboxane production may be a not important factor for determining the increased platelet aggregation which is at the origin of the angiopathy in diabetes mellitus.
Explore the source record for details and available documents.