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Biomedical subjects

H Frerichs

Publications and source records attributed to H Frerichs.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1976

Histochemistry, ultrastructure and hormone content of human insulinomas.

Forty human insulin-producing tumors were investigated with histochemical, immunohistological and ultrastructural methods and extracted for insulin and proinsulin. These studies resulted in the following findings: 1) A variable number of tumor cells contained only a few or often no beta granules. 2) The insulin concentration was lower and the proinsulin percentage higher in insulinoma cells compared with normal beta-cells. 3) According to the ultrastructural appearance of the secretory granules four types of insulinoma were established. 4) Insulinomas frequently contained cells with atypical secretory granules which were Grimelius silver-positive. Their similarity to the Type IV islet cell and to cells regularly found in gastrinomas, Verner-Morrison tumors and glucagonomas suggests that all endocrine pancreatic tumors originate from a common precursor cell. 5) The morphological and biochemical findings support the theory that uncontrolled hormone release and/or decreased storage capacity are responsible for fasting hyperinsulinism in insulinoma patients. 6) The severity of hypoglycemia symptoms and the result of stimulatory tests were not related to the size, the insulin concentration and the total insulin content of the tumor.

Adenoma, Islet Cell↗
PubMed1975

[Secretion of insulin. Hypotheses at present under discussion (author's transl)].

Proinsulin is dissociated into insulin and C-peptide in the Golgi zone and in the beta-granules which fulfil a storage and transport function at the same time. Through an active transport process involving the microtubular and microfilament cytoplasmic system, the granules arrive at the cell wall and there they are emiocytotically excreted. At a still completely unknown spot on this secretory route, control of the secretion rate by calcium ions and cAMP-dependent phosphorylation seems possible. Calcium and cAMP as signal transmitters are again subject to the positive and negative modulating receptor-transmitted effect of adrenergic and cholinergic transmitter substances and beta-cytotropic peptide hormones. The basis of every modulation of the secretory function, however, is a secretion signal dependent on the concentration of glucose itself and glucose metabolites (only one?) on the one hand, and on the other on the energy resulting from endoxidation of glucose in the form of high energy phosphates.

Animals↗
PubMed1975

Tolbutamide-induced changes of the DNA, protein and insulin content and the secretory activity of isolated rat pancreatic islets.

Following prolonged administration of tolbutamide the DNA- and protein content per islet was enhanced but the IRI content per islet was diminished. Glucose-induced (2.0, 8.0 or 16.6 mM) and leucine-induced (12.5 or 25.0 mM) IRI release from isolated islets, as well as 14C02-production from U-14C glucose, were decreased. Theophylline (5.0 mM) restored the glucose sensitivity of the islets towards normal. The results indicate that tolbutamide-induced islet cell hyperplasia does not entail islet hyperfunction, as previously thought. Decreased IRI release may partially be explained by a tolbutamide-induced alteration of the adenylate cyclase/phosphodiesterase system of the B-cell.

Animals↗
PubMed1975

Gastric inhibitory polypeptide: effect on glucose-induced insulin release from isolated rat pancreatic islets in vitro.

Gastric Inhibitory Polypeptide (GIP; 1 or 10 mug/ml) potentiated glucose-induced (8 or 16.6 mM) insulin (IRI) release from isolated rat pancreatic islets. Basal release was unaffected. The threshold concentration of glucose necessary for GIP to modulate IRI release was between 6 and 8 mM. GIP had no effect on IRI release from islets submitted to a maximal glucose stimulus (25 mM).

Animals↗