Biomedical subjects
Publications and source records attributed to H J Hahn.
Somatostatin inhibits in a dose-dependent manner the glucagon secretion in the presence of up to 5 mM glucose, whereas the suppressed glucagon release in the presence of greater than or equal to 10 mM glucose, 10 mM glyceraldehyde, 30 mM fructose or 30 mM mannose is characterized by an increase of hormone release under the influence of somatostatin.
Release of immunoreactive insulin activity (IRI) and biological insulin like activity (ILA) from collagenase isolated pancreatic islets of sand rats (Psammomys obesus) maintained on a vegetable diet were examined at 60 min and 24-48 h intervals under culture conditions at 1.0 and 15.6 mM glucose. The glucose-insulin dose response curves for sand rats after 60 min incubation were compared with those after 24 or 48 h of incubation. The pancreatic islets responded to 5mM glucose with a high insulin release especially under culture conditions. A drastic depletion of stored insulin in the islets cultivated for 2 days at 5 or 15 mM glucose is accompanied by a continuous diminution of the glucose-induced insulin release with the prolongation of cultivation up to one week.
On the basis of the blood glucose increase during the capitivity sand rats born in the desert were classified as normals, protodiabetics and diabetics, indicating a different adaptation to the new environment within a definite period. Isolated islets of animals, which did not develop a hyperglycemia, enhanced their insulin content during the adaptation period. The absolute insulin secretion rates in response to 16.5 mM glucose were rather similar between the three investigated groups and not modified by the insulin as well as glucagon content of pancreatic islets. But, since islets of hyperglycemic sand rats could not increase the insulin content, a significantly enhanced fractional secretion (as % of the content) could be observed. The results let us assume that the B-cell reaction during the adaptation period can be modified by further factors additionally to the changed environment.
Explore the source record for details and available documents.
Isolated pancreatic islets of normoglycemic sand rats do not respond to 2.5 mM glucose with an enhanced glucagon secretion, which could be observed in normal Wistar rats. Arginine stimulates glucagon release in the presence of 2.5 mM glucose in Wistar rats as well as in sand rats. The secretion pattern is not caused by insulin deficiency since sand rat islets are characterized by an increased insulin secretion rate in vitro. This paradoxical glucagon secretion is not caused by a changed glucagon content but might be related to this species which is able to develop a diabetic syndrome spontaneously.
Pancreatic islets of Wistar rats were prepared by digestion with collagenase and then washed and isolated at three different temperatures (4, 22 and 37 degrees C). The efficiency of washing with regard to proteolytic and collagenolytic activities in the wash buffer was not affected by the temperatures used. The islet thiol:protein-disulphide oxidoreductase activity (EC 1.8.4.2) was apparently unchanged, whereas washing temperatures lower than 37 degrees C resulted in a diminished insulin content. The insulin secretion of islets, isolated at 4 degrees C, is reduced in response to glucose without changing the sigmoidal shape of dose-response curve.
The glucose utilization by different skeletal muscle tissues of short-term streptozotocin treated Wistar rats was studied both in vivo and in vitro. The findings permit the following statements: The reduced metabolic conversion of glucose is mainly the result of the diminished transport of glucose into the muscle cells. The utilization of the glucose taken up by the muscle cells for synthesis of glycogen is unchanged in the diabetic animals and can be stimulated by insulin correspondingly as in normal rats. The conversion of the glucose metabolized by the cells to lactate and the time course of the specific activity of glycogen and lactate lead to the conclusion that glycogenolysis in the muscles of streptozotocin diabetic rats during the incubation is enhanced.
Pancreatic islets of wistar rats, isolated after 15 min of digestion with collagenase, secreted insulin in response to 15.0 mM glucose within 2 min and showed the typical sigmoidal glucose response during an incubation time of 15 and 60 min, respectively. Islets, isolated after 35 min of digestion with collagenase, responded with delay after stimulation with glucose (after 15 min of incubation), and are characterized by an increased "release" in the presence of 2.5 mM glucose.
In normoglycemic sand rats the insulin secretion of isolated islets was investigated dependent on the time of artificial nutrition in captivity. Whereas the islets of short-term adapted animals did not respond within 15 min with an enhanced insulin secretion after stimulation with 16.5 mM glucose or 10 mM arginine, prolongation of incubation time resulted in a significantly enhanced hormone release. An intraveneous glucose injection (1 g/kg body weight) 45 min prior to the excision of the pancreas caused an immediate insulin secretion of the isolated islets in response to glucose or arginine. Islets of sand rats adapted for more than 10 weeks to artificial nutrition responded immediately with an enhanced insulin release in contrast to the islets of short-term adapted animals. These differences could not be correlated to the insulin content, the A/B cell ratio, and ultrastructural alterations of the islets.
Insulin (IRI) secretion pattern of collagenase isolated islets from Wistar rats were investigated in a batch type incubation (60 min) and under organ culture conditions (up to 7 days) with different concentrations of glucose as stimulus. The B-cell response within 60 min of incubation was determined in Krebs-Ringer bicarbonate buffer with 1 mg/ml bovine serum albumin and 16 mM HEPES (KRB-HEPES) and compared with the hormone release in a culture medium (TC 199) containing 10% calf serum. Additionally the insulin content of islets before and after 7 days of culture was assayed radioimmunologically. In the presence of culture medium the insulin secretion was enhanced by 5.8 mM glucose whereas this glucose concentration does not stimulate the insulin secretion in KRB-HEPES. During organ culture the insulin secretion was identical in media with 1.0 and 5.8 mM glucose, respectively, but 15 mM glucose raised the hormon output more than 10-fold. The insulin content of islets, cultured for 7 days was decreased in the presence of 15 mM glucose up to 30% and in the presence of 5.8 mM glucose up to 13% of that of islets after isolation. The recovery rate of insulin calculated as the sum of secretion and content after cultivation at 15 mM glucose was higher than 100%, whereas the experiments in the presence of 1.0-5.8 mM glucose are characterized by a recovery rate of 25%. The results are discussed in connection with a altered intracellular breakdown of insulin in the B-cells.
The morphological alterations of B-cells of pancreatic islets from rats were investigated 2, 8 and 24 h after a peroral application of glibenclamide. All cell organelles showed signs of activation, as enlargement of the rough endoplasmatic reticulum and the Golgi apparatus, increased number of mitochondriae and degranulation. These changes could be observed partly 2 h after glibenclamide, but the drastical alterations were found 24 h after application of the sulfonylurea.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.