Search PubMed⌕ Search

Biomedical subjects

H Frerichs

Publications and source records attributed to H Frerichs.

At least 19 recordsLinked to original sources
PubMed1980

Increased somatostatin secretion from pancreatic islets of streptozotocin-diabetic rats in response to glucose.

Glucose stimulates somatostatin release from perifused pancreatic islets of diabetic rats 42-47 days after the induction of diabetes, and 48 h after withdrawal of insulin replacement therapy. The glucose effect is augmented by theophylline or glucagon. Basal somatostatin release and glucose-induced secretion are significantly higher in diabetic islets than in controls. It is suggested that glucose promotes somatostatin release by directly interacting with islet D cells but not via indirect pathways. Glucose-induced stimulation appears to be modulated by a D-cell adenylate cyclase/phosphodiesterase system. Reasons responsible for increased somatostatin secretion by diabetic islets include reduction in B-cell mass, suggesting that B cells may normally suppress the secretory activity of D cells.

Animals↗
PubMed1979

Impaired feedback control of fat induced gastric inhibitory polypeptide (GIP) secretion by insulin in obesity and glucose intolerance.

To investigate the role of endogenous insulin on the secretion of immunoreactive gastric inhibitory polypeptide (IR-GIP) the response of IR-GIP and immunoreactive insulin (IRI) to an oral fat load (100 g triglyceride) alone and during an intravenous glucose infusion (0.7 g/kg/h) was examined in normal weight and obese subjects. In normal weight subjects the fat induced integrated rise of IR-GIP was 112.7 +/- 9.4 ng/ml/120 min. When glucose and fat were given together this IR-GIP response was lowered to 46.2 +/- 2.9 ng/ml/120 min while the serum IRI response to i.v. glucose and the glucose tolerance were enhanced by fat ingestion. In obese subjects with normal glucose tolerance the GIP suppressing effect of i.v. glucose infusion was less marked than in controls. The integrated IR-GIP response to fat ingestion was 225.6 +/- 20.3 mg/ml/120 min and to fat plus glucose 152.6 +/- 14.8 ng/ml/120 min. In obese subjects with glucose intolerance i.v. glucose completely failed to lower the exaggerated secretion of IR-GIP following oral fat. Thus, a graded abnormality of the GIP response to glucose induced insulin release occurs in obesity with normal and pathological glucose tolerance. After reducing the ideal body weight of six obese subjects with glucose intolerance by hypocaloric diet for 3 weeks the exaggerated rise of IR-GIP after oral fat was reversed and the lowering effect of i.v. glucose on the IR-GIP response re-established.

Adult↗
PubMed1979

Effect of fasting on the release of insulin and somatostatin from perifused islets of Langerhans.

Release of somatostatin and insulin from perifused islets of fasted and control rats was compared. After a fasting period of 48 h glucose-induced insulin release but not somatostatin release was diminished. Islets from fasted rats released significantly more somatostatin in the presence of 3.3 mM glucose than islets from controls. Simultaneously, the somatostatin content of isolated islets from fasting rats was significantly decreased. The results indicate that the low secretory activity of islet B cells in the fasting state is associated with a high secretory activity of islet D cells.

Animals↗
PubMed1978

Comparison of alpha-ketoisocaproic acid and glucose in rats: effects on insulin and somatostatin release and on islet cAMP content.

The insulinotropic effects of alpha-ketoisocaproic acid and glucose reveal many common characteristics in vivo and in vitro. They qualify as initiators of insulin release, their action is amplified by potentiators of insulin release, and they have a similar potency at equimolar concentrations. The dynamics of insulin release evoked by alpha-ketoisocaproic acid and glucose are similar. Epinephrine completely inhibits the insulinotropic effect of glucose and alpha-ketoisocaproic acid. Mannoheptulose exhibits a complete, immediate and reversible blockade of glucose-induced insulin release. In contrast, inhibition of alpha-ketoisocaproic acid-induced insulin release occurs after a lag period and is not reversed by removal of the inhibitor. alpha-ketoisocaproic acid, at equimolar concentrations, is several-fold more effective than glucose in elevating cAMP content in islet. alpha ketoisocaproic acid and glucose are about equally effective in stimulating somatostatin release from isolated rat pancreatic islets. This stimulation is inhibited by epinephrine. Mannoheptulose inhibits only somatostatin release induced by glucose but not by alpha-ketoisocaproic acid. It suggested that the insulinotropic characteristics of glucose and alpha-ketoisocaproic acid reveal many common features, while their mode of action appears to be different.

Animals↗
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

Onset and reversibility of changes in secretory function and composition of isolated rat pancreatic islets following long-term administrationof high or low tolbutamide doses.

Chronic administration of a high tolbutamide dose to rats induces islet hypertrophy associated with a decreased insulin content per islet and with a diminished insulin release in response to a glucose or leucine stimulus. These changes are reversible after discontinuation of tolbutamide. Chronic administration of a low tolbutamide dose (effective on islet size, on insulin content per islet, or on leucine-induced insulin release is normal in the presence of glucagon (5 mug/ml) or theophylline (5 mM). Since islet hypertrophy occurs following administration of high tolbutamide doses only and is associated with hypofunction rather than with hyperfunction, it seems hardly conceivable that the therapeutic principle of tolbutamide is based on a beta-cytotrophic effect. B-cell hypofunction seems to be due to at least three factors: the decrease in the insulin content per islet, an impairement in secretory signal recognition, and an interference with the process of signal transmission.

Animals↗
PubMed1976

Cytochalasin B: evidence for a membrane-directed action in B-cells from rat pancreatic islets.

In the presence of cytochalasin B (CCB) concentrations from 50 to 200 mug/ml there is a dose-dependant inhibition of insulin release from isolated rat pancreatic islets. Inhibition is unspecific with respect to glucose, leucine, tolbutamide or theophylline and is reversible. Production of 14CO2 from uniformly labeled D-glucose is decreased. Islets pretreated with an high (200 mug/ml) or low (10 mug/ml) CCB dose release more insulin in response to a subsequent glucose or leucine stimulus in a CCB free medium compared with controls. The data are compatible with a membrane-directed action of CCB.

Animals↗