Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:034761 (insulin)
 211,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric acid output, blood-glucose, serum-gastrin and psychomotor-performance were measured in four healthy subjects one hour before and two hours after the intravenous injection of (a) 2ml saline, (b) 0.2 U/kg b.w. insulin, (c) 0.1 mg/kg b.w. bromazepam. Each subject underwent one experiment of each type. The study was layed out as a Latin-square and analysed accordingly. Gastric acid secretion was measured by means of intragastric titration and a telemetering capsule; blood-glucose and serum-gastrin levels as well as psychomotor performance as a measure of vigilance were determined in 15-minute-intervals. In the saline series (a), none of the four parameters showed any systematic variation. In series (b), a bimodal response of acid output to insulin, initial inhibition and subsequent stimulation was observed in all subjects. Serum-gastrin levels showed only a slight and transient increase in the first thirty minutes. Psychomotor performance decreased markedly with progressing hypoglycemia, and increased when glucose levels rose again. In the bromazepan series (c), acid output and psychomotor performance decreased and, after the first hour, increased almost parallely, while glucose and gastrin levels remained unchanged. In series (d), an additive effect of insulin and bromazepam occurred: acid output and psychomotor performance were lower than after insulin alone; peak acid secretion, maximal hypoglycemia and peak of serum-gastrin were shifted to the right. It is concluded that the lowered basal as well as insulin-stimulated acid secretion after bromazepam is due to the central effect of the drug, and that this effect is mediated to the gastric glands directly via autonomic nervous pathways without involving a release of endogenous gastrin.
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PMID:Gastric acid secretion, serum-gastrin levels and psychomotor function under the influence of placebo, insulin-hypoglycemia, and/or bromazepam. 0 60

Melanocyte Release-Inhibiting Peptide (MRIP-I) did not affect circulating levels of ACTH, LH, FSH, TSH,ORL, betaMSH and insulin when iv infused (5.0 mg in 5 min plus 0.4 mg/min for 70-115 min), while it significantly reduced serum GH response to hypoglycemia in normal subjects and lowered serum GH levels in acromegalics. There was no correlation between the fall in serum GH after MRIP and after dopaminergic drugs in acromegaly. These data are compatible with either a direct suppressive action exerted by MRIP-I at pituitary level or an extra-pituitary effect not involving dopaminergic pathways. It can be spec-lated that since labelled MRIP-I accumualtes in the pineal and melatonin blunts GH response to hypoglycemia, the pineal gland might be involved in the MRIP-I-induced suppression of GH secretion.
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PMID:Influence of L-prolyl-L-leucyl-glycine amide on growth hormone secretion in normal and acromegalic subjects. 0 65

Sequential determinations of glucose outflow and inflow, and rates of gluconeogenesis from alanine, before, during and after insulin-induced hypoglycemia were obtained in relation to alterations in circulating epinephrine, norepinephrine, glucagon, cortisol, and growth hormone in six normal subjects. Insulin decreased the mean (+/-SEM) plasma glucose from 89+/-3 to 39+/-2 mg/dl 25 min after injection, but this decline ceased despite serum insulin levels of 153+/-22 mul/ml. Before insulin, glucose inflow and outflow were constant averaging 125.3+/-7.1 mg/kg per h. 15 min after insulin, mean glucose outflow increased threefold, but then decreased at 25 min, reaching a rate 15% less than the preinsulin rate. Glucose inflow decreased 80% 15 min after insulin, but increased at 25 min, reaching a maximum of twice the basal rate. Gluconeogenesis from alanine decreased 68% 15 min after insulin, but returned to preinsulin rates at 25 min, and remained constant for the next 25 min, after which it increased linearly. A fourfold increase in mean plasma epinephrine was found 20 min after insulin, with maximal levels 50 times basal. Plasma norepinephrine concentrations first increased significantly at 25 min after insulin, whereas significantly increased levels of cortisol and glucagon occurred at 30 min, and growth hormone at 40 min after insulin. Thus, insulin-induced hypoglycemia in man results from both a decrease in glucose production and an increase in glucose utilization. Accelerated glycogenolysis produced much of the initial, posthypoglycemic increment in glucose production. The contribution of glycogenolysis decreased with time, while that of gluconeogenesis from alanine increased. Of the hormones studied, only the increments in plasma catecholamines preceded or coincided with the measured increase in glucose production after hypoglycemia. It therefore seems probable that adrenergic mechanisms play a major role in the initiation of counter-regulatory responses to insulin-induced hypoglycemia in man.
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PMID:The role of adrenergic mechanisms in the substrate and hormonal response to insulin-induced hypoglycemia in man. 0 91

The effects of atenolol, a new beta1-blocking drug, on pulse rate, sweating, and blood glucose levels during insulin-induced hypoglycaemia were studied in a double-blind crossover trial in eight normal subjects using placebo and propranolol as reference agents. The intensity of induced hypoglycaemia was identical for atenolol, propranolol, and placebo. Propranolol prolonged hypoglycaemia, but atenolol did not. Atenolol may therefore be safe for use in patients receiving insulin.
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PMID:Comparison of atenolol and propranolol during insulin-induced hypoglycaemia. 0 84

Metoprolol and acebutolol, two supposedly cardio-selective beta-adrenergic recptor blocking agents, were tested in healthy volunteers against propranolol, a non-selective drug, for their effect on blood glucose levels during insulin-induced hypoglycaemia. There was not significant difference between propranolol and metoprolol, which both potentiated the initial hypoglycaemic action of the insulin and delayed the return to normoglycaemia. Acebutolol, even though potentiating the initial hypoglycaemia, did not possess a significant delaying effect. A similar trial should be undertaken in diabetics to determine with certainty the safety of such drugs in diabetes mellitus.
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PMID:Comparison of propranolol, metoprolol, and acebutolol on insulin-induced hypoglycaemia. 0 87

The effect of insulin-induced hypoglycemia on the blood levels of catecholamines and renin activity has been studied in five patients with moderate hypertension before and after treatment for 3 - 8 months with penbutolol (PEN) 20 - 30 mg twice daily. Penbutolol caused no change in fasting blood glucose level. Insulin o.1 IU per kg body weight i.v. reduced blood glucose concentration by approximately 50 per cent after 30 - 45 min, both before and during treatment with penbutolol. Hypoglycemia prior to medication was accompanied by a marked increase in the production of adrenaline and a minor increase of noradrenaline in all five patients. During treatment the response of adrenaline to hypoglycemia was reduced in four patients and the data was inconclusive in one. Basal renin activity was rather low in three patients, within the normal range in one and relatively high in one. Before penbutolol the hypoglycemia-induced increase in catecholamine production caused no change in plasma renin activity in the three patients with low basal levels, whereas a marked increase was observed in the other two. During medication plasma renin activity remained unchanged on induction of hypoglycemia regardless of the catecholamine response. Despite the marked increase in plasma adrenaline following insulin-induced hypoglycemia, no statistically significant increase in pulse rate was recorded.
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PMID:Long term treatment of moderate hypertension with penbutolol (Hoe 893d). II. Effect on the response of plasma catecholamines and plasma renin activity to insulin-induced hypoglycemia. 0 1

13 patients, nine women and four men, aged 22 to 83 years, were treated for diabetic coma or precoma between September 1974 and January 1976. Ten patients were known diabetics and six of them had been treated with insulin. On admission blood sugar was 32.4 +/- 3.3 mmol/l (5.84 +/- 0.6 g/l). The capillary blood pH was 7.15 +/- 0.06 (n = 13). Treatment consisted of continuous insulin infusion (6 IU soluble insulin/hour), physiological saline, potassium substitution and sodium bicarbonate (if the pH was below 7.15). In the first hours of treatment 98 +/- 12IU of insulin, 6.5 +/- 0.5 litres of fluid, 168 +/- 22 mmol of potassium and 237 +/- 55 mmol NaHCO3 were required. During the first 4 hours of the insulin infusion the blood sugar decrease per hour was 3.55 mmol/l (0.64 g/l). Hypokalaemia during treatment occurred in one case, hypoglycaemia was not observed. A preceding treatment with insulin and severe acidosis did not influence therapeutic success. Twelve patients were treated successfully, one patient died 6 hours after admission following mesenteric arterial embolism.
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PMID:[Treatment of diabetic coma and precoma with continuous low-dose insulin infusions (author's transl)]. 1 Oct 87

Insulin, proinsulin, glucagon and gastrin were determined in extracts of tumors of 27 patients with pancreatic islet cell neoplasia of pancreas, in one patient with nesidioblastosis, in extracts of uninvolved portions of the pancreas in 11 of the tumor patients and of 15 control pancreases. Mean insulin concentration in solitary adenomas and in adenomas of patients with adenomatosis was higher than in control pancreases; however, in all but 1 patient the insulin concentration in neoplastic islet tissue was lower than in islet tissue of control pancreas, assuming islet volume is 1% of pancreas. The percentage of proinsulin was elevated in 52% of tumors. Adenoma insulin content correlated with increments of plasma insulin after tolbutamide administration. Insulin and proinsulin concentrations in pancreas uninvolved by tumor were not suppressed. Fasting plasma glucagon was elevated in patients with islet cell adenomatosis and in patients with islet cell carcinoma some of whom had multiple endocrine adenomatosis. The mean concentration of glucagon in tumors was lower than in control pancreases. Elevated concentration of gastrin was found in some adenomas. The data indicate: 1) insulin-secreting islet cell tumors have decreased storage capacity for insulin, 2) elevated concentration of proinsulin in tumors may be due to decreased capacity to store insulin and in some to decreased conversion of proinsulin to insulin as well, 3) tolbutamide stimulates the exaggerated release of a relatively constant fraction of insulin stored in adenomas. 4) solitary adenomas may contain excess amounts of pancreatic hormones in addition to insulin, 5) elevated plasma glucagon in patients with organic hyperinsulinism may indicate malignancy, microadenomatosis or multiple endocrine adenoma syndrome, and 6) chronic hyperinsulinism and hypoglycemia due to adenoma do not suppress insulin and proinsulin content of uninvolved pancreas.
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PMID:Insulin, proinsulin, glucagon and gastrin in pancreatic tumors and in plasma of patients with organic hyperinsulinism. 1 70

The gastric acid response to i.v. injection of 0.15 U of soluble insulin/kg b.w. was determined in healthy subjects and duodenal ulcer patients during intragastric perfusion with water, 0.1 M HC1, and alkaline buffer (pH 8.3). Perfusion with hydrochloric acid significantly reduced the peak gastric acid output following insulin in 6 healthy subjects (reduction 45%, p less than 0.05) but had no significant effect on the peak gastric acid response to insulin in 7 DU patients (reduction 16%, p greater than 0.05). The 2.5-hour gastric acid response to insulin was, however, significantly reduced in both groups (56% and 35%, respectively) by exogenous acidification of the stomach. The gastric acid response to insulin hypoglycaemia in 3 DU patients was the same with intragastric water and alkaline buffer perfusion. The reduction of the gastric acid response to insulin hypoglycaemia by intragastric acidification corresponded to a reduced volume secretion and could not be ascribed to increased back diffusion of hydrogen ions or duodenal inhibition. These findings suggest that the gastric acid response to insulin hypoglycaemia is inhibited by a low intragastric pH in man, and that DU patients are less sensitive to the inhibitory mechanism than healthy subjects.
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PMID:The effect of intragastric pH-variations on the gastric acid response to insulin hypoglycaemia in healthy subjects and duodenal ulcer patients. 1 11

Acid-reflux studies were carried out in 10 healthy subjects in the basal state, during continuous infusion of pentagastrin (0.015 mug/kg body-weight) after bolus injection of insulin (0.2 IU/kg bodyweight), and after intragastric instillation of 200 ml hydrochloric acid. Basal gastro-oesophageal sphincter pressure and rise in intragastric pressure on leg raising were measured by means of perfused catheters. The increase of intragastric acidity during infusion of pentagastrin and during insulin-induced hypoglycaemia was not accompanied by changes in the competence of the gastro-oesophageal region. Instillation of hydrochloric acid was followed by a significant enhancement of the reflux tendency. Changes in intragastric pressure-rise were not demonstrated in any of the series of investigation. Gastric acid secretion and its significance at the evaluation of the results of reflux studies by means of pH-measuring equipment has not been clarified in patients. It can therefore reasonably be demanded of future acid reflux studies that details have to be stated with regard to acid secretion, and that these should be taken into account at the assessment of the results of the study.
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PMID:Effect of changes in the intragastric milieu on competence of the gastro-oesophageal region. A study in normal subjects. 1 13


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