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Biomedical subjects

V Maier

Publications and source records attributed to V Maier.

At least 55 records · Page 3Linked to original sources
PubMed1983

Effects of synthetic rat C-peptide in normal and diabetic rats.

The effects of synthetic rat C-peptide 1 and C-peptide 2 on plasma insulin and blood glucose concentrations in the rat were studied. Infusion of rat C-peptide (500 micrograms X h-1 X kg-1) diminished glucose induced increase of plasma insulin by 56% (15.2 +/- 0.9 versus 6.6 +/- 0.6 ng/ml, p less than 0.01, mean +/- SEM). Somatostatin infused at a rate of 50 micrograms X h-1 X kg-1 body weight inhibited glucose-induced insulin secretion by 33%. In the presence of a mixture of both C-peptides or somatostatin, blood glucose after intravenous glucose was higher than in the control experiments. In alloxan-diabetic rats, C-peptide (160 micrograms/kg) significantly increased and prolonged the hypoglycaemic effect of exogenous insulin. It is suggested that C-peptide may not be a biologically inert substance.

Animals↗
PubMed1983

Carbohydrates modulate opiate receptor mediated mechanisms during postprandial endocrine function.

The present study was designed to determine the role of carbohydrates during naloxone-induced opiate receptor blockade upon the postprandial rise of plasma somatostatin (SLI), insulin and pancreatic polypeptide (PP) levels in response to protein and fat test meals in conscious dogs. Test meals consisting of 50 g liver extract + 50 g sucrose or 50 g corn oil + 50 g sucrose dissolved in 300 ml water were instilled intragastrically, respectively. Additionally, liver extract and fat meals were given with a concomitant intravenous infusion of glucose. To all test meals either naloxone (4 mg) or saline was added. The addition of sucrose to liver extract or the infusion of i.v. glucose during the liver meal abolished the inhibitory effect of naloxone on the rise of postprandial somatostatin levels which has been described recently. The addition of carbohydrate either orally or intravenously to the fat meal resulted in an even stimulatory effect of naloxone upon the rise of postprandial somatostatin levels. Insulin levels were not changed during liver extract + sucrose or i.v. glucose, respectively. When sucrose or i.v. glucose was administered together with the fat meal the addition of naloxone augmented postprandial insulin secretion. Pancreatic polypeptide (PP) release was augmented during the combination of sucrose or i.v. glucose with the fat and liver meal when naloxone was present in the meals. The present data demonstrate that the addition of carbohydrates either orally or intravenously to fat and protein meals modulates the effect of endogenous opiates in the regulation of postprandial somatostatin, insulin and pancreatic polypeptide release in dogs in a way that carbohydrates induce inhibitory mechanisms that are mediated via endogenous opiate receptors.

Animals↗
PubMed1983

Evidence for a role of endogenous opiates in postprandial somatostatin release.

Previously, we have demonstrated the effects of exogenously administered opiates on somatostatin release in dogs and therefore the present study was designed to determine the effect of endogenous opiates via naloxone-induced opiate receptor blockade on somatostatin release. Additionally, plasma insulin and pancreatic polypeptide (PP) levels were determined in response to intragastrically instilled protein, carbohydrate and fat test meals in a group of eight conscious dogs. To all test meals either naloxone (4 mg) or saline was added. The rise of plasma somatostatin levels in response to liver extract, sucrose and fat was attenuated significantly by naloxone. Naloxone had no effect on the rise of postprandial plasma insulin and PP levels. The present data demonstrate that endogenous opiates have a stimulatory effect on postprandial somatostatin release in dogs which indicates a tight interaction that might be of relevance for nutrient homeostasis.

Animals↗
PubMed1983

Acoustic imprinting leads to differential 2-deoxy-D-glucose uptake in the chick forebrain.

This report describes experiments in which successful acoustic imprinting correlates with differential uptake of D-2-deoxy[14C]glucose in particular forebrain areas that are not considered primarily auditory. Newly hatched guinea chicks (Numida meleagris meleagris) were imprinted by playing 1.8-kHz or 2.5-kHz tone bursts for prolonged periods. Those chicks were considered to be imprinted who approached the imprinting stimulus (emitted from a loudspeaker) and preferred it over a new stimulus in a simultaneous discrimination test. In the 2-deoxy-D-glucose experiment all chicks, imprinted and naive, were exposed to 1.8-kHz tone bursts for 1 hr. As shown by the autoradiographic analysis of the brains, neurons in the 1.8-kHz isofrequency plane of the auditory "cortex" (field L) were activated in all chicks, whether imprinted or not. However, in the most rostral forebrain striking differences were found. Imprinted chicks showed an increased 2-deoxy-D-glucose uptake in three areas, as compared to naive chicks: (i) the lateral neostriatum and hyperstriatum ventrale, (ii) a medial magnocellular field (medial neostriatum/hyperstriatum ventrale), and (iii) the most dorsal layers of the hyperstriatum. Based on these findings we conclude that these areas are involved in the processing of auditory stimuli once they have become meaningful by experience.

Acoustic Stimulation↗
PubMed1982

Effect of histamine H2-receptor stimulation on postprandial pancreatic and gastric endocrine function in dogs.

The effect of histamine H2-receptor stimulation via the infusion of impromidine was assessed with regard to postprandial plasma insulin, pancreatic polypeptide (PP), somatostatin, and gastrin levels. The effect of impromidine was assessed in the postprandial state during a liver extract/sucrose test meal which had a buffer capacity to maintain the intragastric pH at a constant level for the time impromidine was infused. Postprandial plasma insulin and gastrin levels were not changed by impromidine (10 micrograms/kg X h-1). Plasma somatostatin levels rose significantly, whereas the postprandial increase of plasma PP levels was attenuated. The effects on somatostatin and PP were antagonized by the infusion of cimetidine, a specific histamine H2-receptor blocker. In conclusion the present data demonstrate that in the postprandial state activation of H2-receptors stimulates somatostatin and inhibits PP release while insulin and gastrin release are not affected.

Animals↗
PubMed1981

Effect of physiological increments of blood glucose on plasma somatostatin and pancreatic polypeptide levels in dogs.

The present study was designed to determine the effects of physiological increments of plasma glucose levels upon basal and stimulated plasma somatostatin and pancreatic polypeptide levels. In seven conscious dogs the elevation of plasma glucose levels by 30-40 mg/dl did not change basal somatostatin and pancreatic polypeptide levels. During stimulation of these two hormones by acetylcholine and the octapeptide of cholecystokinin intravenous infusion of glucose elicited a significant decrease of somatostatin levels by 30 pg/ml and of pancreatic polypeptide levels by 300 pg/ml. The present data demonstrate that a physiological elevation of plasma glucose levels inhibits stimulated but not basal somatostatin and pancreatic polypeptide levels which may be of importance for nutrient entry and metabolism.

Acetylcholine↗
PubMed1979

D-Trp8-D-Cys14-somatostatin--demonstration of its differential suppressive activity in juvenile diabetics.

In 8 insulin-dependent diabetics, the effect of D-Trp8-D-Cys14-somatostatin on blood glucose, growth hormone, and glucagon levels as well as on insulin requirements from an artificial endocrine pancreas was studied during a balanced meal. The somatostatin analogue was infused at a rate of 25 microgram/h preceeded by a bolus injection of 25 microgram 30 minutes before ingestion of the meal. At this dose the analogue had no effect on glucagon levels and insulin requirements from the artificial pancreas. On the other hand, there was a significant lowering effect on fasting blood glucose levels, possibly indicating a direct inhibition of hepatic glucose production. Furthermore, there might be a slight effect on growth hormone levels, as was demonstrated by a rebound increase after termination of analogue infusion.

Adolescent↗
PubMed1979

Influence of insulin infusion kinetics of an artificial beta cell on blood glucose control in insulin-dependent diabetics.

The influence of different control modes for insulin infusion with an artificial beta cell was examined in 41 insulin-dependent diabetics. In 21 Patients, oral glucose tolerance tests were performed with control modes characterized either by low dynamic and high static gain (type I, 10 patients) or high dynamic and low static gain (type III, 11 patients). The change from type I to type III control mode effected an increase of initial insulin infusion rates (91 +/- 59 to 313 +/- 81 mU/min 10-20 min after glucose ingestion) and a decrease of infusion rates during the following phase of the 3-hour observation period (28.2 +/- 4.2 to 18.1 +/- 2.8 U) in patients whose blood glucose curves were completely normalized. Suppression of plasma glucagon levels, observed in 5 healthy control subjects, was not fully restored to normal in these patients. In another 20 insulin-dependent diabetics, daily insulin requirements form the artificial beta cell were determined by employing two control modes (types II and III) comparable in static control but different in dynamic control. Gain of dynamic control, especially in the range of falling glucose levels, was higher in type III control mode (15 patients) than in type II mode (5 patients). These insulin requirements were compared to the insulin doses necessary for subcutaneous treatment. While intravenous insulin requirements were much higher when type II control mode was employed (78.2 +/- 10.2%), during application of type III mode, intravenous insulin requirements were only 10.8 +/- 5.5% higher than subcutaneous doses. We conclude from these data that early increases in insulin infusion rates followed by a rapid decrease seem to reduce insulin requirements after glucose ingestion. A high-gain dynamic control is the basis for this insulin infusion profile.

Adolescent↗
PubMed1979

The effect of three days of blood glucose normalization by means of an "artificial endocrine pancreas" on the concentrations of growth hormone, glucagon, and cortisol in juvenile diabetics.

Glucagon, growth hormone, and cortisol secretion was studied in seven male insulin-dependent diabetics under conventional subcutaneous insulin therapy and after three days of blood glucose normalization attained by the artificial endocrine pancreas (Biostator-GCIIS). The diurnal hormonal profiles under the two types of therapy were compared. Six healthy male students served as control group. A three-day period of blood glucose normalization in insulin-dependent diabetic can restore glucagon secretion to normal. Growth hormone secretion is decreased but not completely normalised. Cortisol secretion is slightly decreased. It is concluded that prolonged normoglycemia achieved by means of an artificial endocrine pancreas may completely control endocrine abnormalities in insulin-dependent diabetics.

Adult↗
PubMed1978

Transmitter mediated arginine vasopressin release from superfused hypothalamus and pituitary gland.

The study was designed to investigate the effect of various neurotransmitters on the hypothalamus and pituitary gland to determine the sites of their action. Superfused isolated rat hypothalami and pituitary glands demonstrated basal secretion of arginine vasopressin (AVP) and repeated response to stimulation thus showing the viability of the preparation. Acetylcholine and histamine stimulated the release of AVP at the hypothalamic and pituitary levels; dopamine and norepinephrine released AVP in a dose related manner only from the hypothalamus; angiotensin II released AVP in the same fashion only from the pituitary gland. AVP secretion stimulated by dopamine and norepinephrine may represent synaptic inputs which are localized at the hypothalamus and must be distinguished from the site of action at the pituitary gland of angiotensin II.

Acetylcholine↗
PubMed1977

Insulin release from collagenase-isolated islets of rat pancreas in the presence of cyclic AMP and somatostatin.

In order to study the role of cyclic AMP in the inhibition by somatostatin of glucose-induced insulin release, the effect of somatostatin on the potentiation by dibutyryl-cyclic AMP (db-cAMP) of insulin release from isolated pancreatic islets of rats was examined. Isolated islets were obtained from the rat pancreas by the collagenase method. Ten islets were incubated for periods of 30 min in Krebs-Ringer bicarbonate buffer containg albumin and glucose 2.0 mg/ml in the presence or absence of somatostatin (1 microgram/ml or 100 ng/ml) and/or db-cAMP 1 mM. Glucose-induced insulin release was reduced by somatostatin in concentrations of 1 microgram/ml. Somatostatin in a concentration of 100 ng/ml significantly abolished the potentiation by db-cAMP of insulin release (p less than 0;01), in spite of exerting no inhibition of glucose-induced insulin release. However, in the presence of theophylline 5 mM, somatostatin 100 ng/ml did not show that inhibitory effect on the potentiated insulin release.

Animals↗
PubMed1977

Improved method and its clinical application of a radioimmunoassay of arginine vasopressin in human serum.

A sensitive and specific double-antibody radioimmunoassay for measuring circulating levels of arginine vasopressin in human serum is described. It is possible to detect arginine vasopressin levels of 1 microU/ml serum without extraction procedure. Normal subjects were found to have 5.7 +/- 4.4 microU/ml after a dehydration period of 12 hours. Water loading diminished arginine vasopressin concentrations while dehydration increased it. Application of furosemide over a period of 14 days brought forth constant but not significant decreases. Subjects suffering from psychogenic polydipsia showed normal levels in spite of drinking 8-12 liters of water per day. Patients suffering from liver cirrhosis with ascites showed significantly higher arginine vasopressin levels, approaching normal values, when ascites was under control.

Arginine Vasopressin↗
PubMed1975

Interactions of concanavalin A with isolated pancreatic islets.

Pancreatic islets of mice were isolated by the collagenase method. After a preincubation period of 20 min they were incubated in Krebs-Ringer-albumin buffer in the presence of glucose. Concanavalin A (2 mg/ml) inhibits the glucose-induced release of insulin; this same property is shown by Concanavalin A bound to nonphagocytosable beads of Sephrose at lower concentrations (0.4 mg/ml). In pancreatic islets stimulated by tolbutamide, glibenclamide or arginine the secretion of insulin is not inhibited in the presence of Concanavalin A. The incorporation of tritiated leucine is not influenced by Concanavalin A. Since desialized pancreatic islets react in the same way the glucose-induced secretion of insulin appears to be a membrane-dependent process.

Animals↗