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Biomedical subjects

R Ebert

Publications and source records attributed to R Ebert.

At least 109 records · Page 6Linked to original sources
PubMed1978

Assessment of hormone loss through hemofiltration.

The concentrations of testosterone, cortisone, gastrin, insulin, gastric inhibitory polypeptide (GIP), somatomedin B, parathyroid hormone (PTH), human growth hormone (HGH) and thyroid stimulating hormone (TSH) have been determined in the plasma and the ultrafiltrate of five uremic patients undergoing intermittent hemofiltration treatment. There was a considerable loss of gastrin, insulin, GIP, somatomedin B and PTH by hemofiltration treatment. The plasma concentrations, however, did not decrease except for immunoreactive-PTH (IR-PTH) which returned from elevated to normal levels. Cortisone, HGH and TSH concentrations in the ultrafiltrate were below the measureable range. A significant elimination of 11-hydroxylated androstans by hemofiltration may have a positive effect on the disturbed steroid metabolism. Results indicate that hemofiltration does not cause a hormone deficiency syndrome. On the contrary, the loss of degradation products of hormones with disturbing biological activity may be a favorable effect of the hemofiltration treatment.

Cortisone↗
PubMed1978

Serum gastric inhibitory polypeptide (GIP) in duodenal ulcer disease: relationship to glucose tolerance, insulin, and gastrin release.

Serum immunoreactive gastric inhibitory polypeptide (IR-GIP), gastrin (IRG), and insulin (IRI) were estimated in 41 normal weight patients with duodenal ulcer (DU) and 25 age-matched controls in response to a high calorie liquid test meal. 28 out of 41 DU patients had a hyperglycaemic glucose response during the test meal, and 15 had a pathological oral glucose tolerance test. Fasting and food-stimulated IR-GIP and IRG levels were significantly elevated in the DU patients. Serum IRI also increased to significantly higher levels in DU patients after the test meal. The degree of the greater hormone response was dependent on the glucose increase after the test meal in the case of insulin and GIP, but not in the case of gastrin. It is concluded: firstly, that a faster glucose absorption (possibly due to rapid initial gastric emptying or increased intestinal motility) is responsible for the high and short-lasting glucose peak and the increased GIP and insulin secretion; secondly, that the GIP response could well be causally related to the insulin response; thirdly, that hyposcretion of GIP is ruled out as a possible factor in the pathogenesis of gastric acid hypersecretion of duodenal ulcer patients.

Adult↗
PubMed1978

[Gastric inhibitory polypeptide (GIP) (author's transl].

Gastric inhibitory polypeptide (GIP) is released from the duodenum and jejunum following the ingestion of glucose, fat and amino acids. This hormone potentiates the glucose-induced insulin release from the beta-cells of the pancreas. The role of GIP as "incretin" is discussed. The method of the radioimmunoassay for the determination of GIP in serum samples is described. The lower limit of sensitivity of the GIP radioimmunoassay is in the range of 30-50 pg per ml serum. The described radioimmunoassay is sensitive enough to determine fasting levels of GIP in normal subjects (287 +/- 59 pg/ml). The clinical and pathophysiological importance of GIP is discussed by means of various diseases (obesity, maturity-onset diabetes mellitus, duodenal ulcer disease).

Administration, Oral↗
PubMed1977

Permissive effect of glucose on the glucagon-induced accumulation of cAMP in isolated rat pancreatic islets.

Glucose stimulation increased the cAMP content of collagenase-isolated rat pancreatic islets fourfold above baseline values. The elevation was transient, lasting about 5 min, and was dose-dependent. Insulin release continued at a constant rate throughout the incubation. Glucagon, in the absence of glucose, increased cAMP for about 1 min but only slightly, and had no effect on insulin release. In the presence of glucose, however, glucagon enhanced islet cAMP content 15-fold and increased the release of insulin. Glucagon was most effective at high glucose concentrations (16.6 and 25 mM). This indicates that glucagon is critically dependent on the presence of glucose in order to increase the islet cAMP content and to stimulate insulin release. The inability of glucagon to generate sufficient cAMP in the absence of glucose might be one of the reasons why the hormone is a potentiator rather than an initiator of insulin release.

Animals↗
PubMed1977

Lowering of fasting and food stimulated serum immunoreactive gastric inhibitory polypeptide (GIP) by glucagon.

The effect of intravenous glucagon infusion on serum levels of immunoreactive GIP (IR-GIP), insulin (IRI), gastrin (IRG), and on blood glucose has been investigated in six healthy volunteers in the fasting state and during ingestion of a mixed standard meal. Glucagon (500 ng/kg/min) lowered significantly serum levels of IR-GIP and IRG below the fasting values and increased the levels of IRI and blood glucose. Glucagon (50 ng/kg/min) infused 30 minutes before and continued 90 minutes after ingestion of a test meal abolished the IR-GIP response, suppressed significantly the IRG response, and left the IRI response unchanged. The same glucagon dose infused 60 minutes after ingestion of the test meal decreased significantly the raised levels of IR-GIP and IRG to fasting levels without changing IRI values. It is concluded that exogenous glucagon inhibits Gip release at the level of the GIP-producing cells.

Adult↗
PubMed1977

Elimination of hormones through hemofiltration.

The concentrations of testosterone, cortisone, gastrin, GIP, somatomedin B, insulin, HGH, and TSH have been determined in the plasma and the ultrafiltrate of five uremic patients undergoing intermittent hemofiltration treatment. There was a considerable loss of gastrin, GIP, somatomedin B, and insulin by hemofiltration treatment; the plasma concentrations, however, did not decrease. Cortisone, HGH, and TSH were not detectable in the ultrafiltrate. Our results therefore indicate that hemofiltration does not cause a hormone deficiency syndrome. On the contrary, the loss of degradation products of hormones with disturbing biological activity may be a favourable effect of the hemofiltration treatment.

Cortisone↗
PubMed1976

Gastric inhibitory polypeptide (GIP), gastrin and insulin: response to test meal in coeliac disease and after duodeno-pancreatectomy.

The response of serum immunoreactive gastric inhibitory polypeptide (IR-GIP), gastrin (IRG) and insulin (IRI) to a mixed standard meal was measured in 15 controls, 6 patients with coeliac disease, 26 patients with chronic pancreatitis and partial duodenopancreatectomy (Whipple's procedure). Serum levels of IR-GIP, IRG and IRI were significantly reduced in patients with coeliac disease. The serum glucose increase was significantly smaller only during the first hour after the meal. Since small intestinal GIP- and G-cells are situated mainly in the glands of duodenal and jejunal mucosa their absolute number is not significantly reduced in coeliac disease. It is suggested that the release of IR-GIP and duodenal IRG is influenced by the rate of absorption of nutrients. In patients with chronic pancreatitis the IR-GIP release is significantly greater than in controls, the IRG release normal and the IRI response delayed. After Whipple's procedure the IR-GIP response is increased significantly while the IRG secretion is abolished. This demonstrates that the duodenum is not necessary for GIP release and that pancreatic and jejunal gastrin are without clinical significance.

Adult↗
PubMed1976

Response of gastric inhibitory polypeptide (GIP) to test meal in chronic pancreatitis--relationship to endocrine and exocrine insufficiency.

Twenty-nine patients with chronic pancreatitis had a significantly greater IR-GIP response to a test meal than 15 controls. This increased response was not related to the degree of steatorrhoea or glucose intolerance. It was most marked in a group of patients with moderately impaired IRI release and medium steatorrhoea. From this is concluded that the IR-GIP response to a test meal is determined by at least two factors: 1. feedback control via insulin secretion, 2. assimilation of fat. In chronic pancreatitis endocrine insufficiency may induce an exaggerated GIP response and severe exocrine insufficiency may prevent fat induced GIP release. Gastrin is not involved in the different GIP response in patients with chronic pancreatitis.

Adult↗