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Suad Efendic - One of the best experts on this subject based on the ideXlab platform.
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diazepam binding inhibitor and the endocrine Pancreas
Neuropharmacology, 1991Co-Authors: Claes-göran Östenson, Marita Hilliges, Olle Johansson, S Karlsson, Bo Ahrén, Suad EfendicAbstract:Summary Regulation of blood glucose homeostasis is complex. Its major hormonal regulators include insulin, glucagon and somatostatin from the endocrine Pancreas. Secretion of these hormones is controlled predominantly by the supply of nutrients in the circulation but also by nerve signals and other peptides. Thus, it is likely that peptides, released from cells of the gut or endocrine Pancreas or from peptidergic nerves, affect glucose homeostasis by modulating the Secretion of insulin, glucagon and somatostatin. When searching for novel gut peptides with such effects, diazepam binding inhibitor (DBI) was isolated from the porcine small intestine. By immunocytochemistry, DBI has been demonstrated to occur not only in the gut but also in endocrine cells of the pancreatic islets, namely in the somatostatin-producing D-cells in pig and man, and in the glucagon-producing A-cells in rat. Porcine DBI (pDBI; 10 −8 –10 −7 M) has been shown to suppress glucose-stimulated release of insulin from both isolated islets and perfused Pancreas of the rat. Furthermore, Secretion of insulin stimulated by either the sulfonylurea glibenclamide or the phosphodiesterase inhibitor 3-isobutyl-I-methylxanthine (IBMX), was inhibited by the peptide. In contrast, arginine-induced release of insulin was unaffected by pDBI. Moreover, pDBI decreased arginine-induced release of glucagon from the perfused rat Pancreas, whereas release of somatostatin was unchanged. Notably, rat DBI, structurally identical with rat acyl-CoA-binding protein, has also been demonstrated to inhibit glucose-stimulated release of insulin in the rat, both in vivo and in vitro . Long-term exposure of cultured fetal rat islets to pDBI (10 −8 M) significantly decreased the synthesis of DNA in islet cells. In conclusion, DBI moderately suppresses the Secretion of insulin from the B-cells, when stimulated by agents closing ATP-sensitive K + -channels (glucose, glibenclamide) or enhancing the formation of cAMP (IBMX). The mechanism of such an effect is not likely to involve binding of DBI to benzodiazepine-recognition sites of GABA-receptors, since B-cells are reportedly lacking this type of receptor. It cannot be ruled out that the peptide exerts its effect indirectly by binding factors important in regulation of Secretion of insulin, due to its ability to bind amphiphilic compounds. The occurrence of DBI immunoreactivity in non-B-cells of the islets suggests that the peptide may modulate Secretion of insulin locally through paracrine interaction.
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Diazepam binding inhibitor and the endocrine Pancreas.
Neuropharmacology, 1991Co-Authors: Claes-göran Östenson, Marita Hilliges, Olle Johansson, S Karlsson, Bo Ahrén, Suad EfendicAbstract:Regulation of blood glucose homeostasis is complex. Its major hormonal regulators include insulin, glucagon and somatostatin from the endocrine Pancreas. Secretion of these hormones is controlled predominantly by the supply of nutrients in the circulation but also by nerve signals and other peptides. Thus, it is likely that peptides, released from cells of the gut or endocrine Pancreas or from peptidergic nerves, affect glucose homeostasis by modulating the Secretion of insulin, glucagon and somatostatin. When searching for novel gut peptides with such effects, diazepam binding inhibitor (DBI) was isolated from the porcine small intestine. By immunocytochemistry, DBI has been demonstrated to occur not only in the gut but also in endocrine cells of the pancreatic islets, namely in the somatostatin-producing D-cells in pig and man, and in the glucagon-producing A-cells in rat. Porcine DBI (pDBI; 10(-8)-10(-7) M) has been shown to suppress glucose-stimulated release of insulin from both isolated islets and perfused Pancreas of the rat. Furthermore, Secretion of insulin stimulated by either the sulfonylurea glibenclamide or the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), was inhibited by the peptide. In contrast, arginine-induced release of insulin was unaffected by pDBI. Moreover, pDBI decreased arginine-induced release of glucagon from the perfused rat Pancreas, whereas release of somatostatin was unchanged. Notably, rat DBI, structurally identical with rat acyl-CoA-binding protein, has also been demonstrated to inhibit glucose-stimulated release of insulin in the rat, both in vivo and in vitro. Long-term exposure of cultured fetal rat islets to pDBI (10(-8) M) significantly decreased the synthesis of DNA in islet cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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Diazepam binding inhibitor and the endocrine Pancreas.
Neuropharmacology, 1991Co-Authors: Claes-göran Östenson, Marita Hilliges, Olle Johansson, S Karlsson, Bo Ahrén, Suad EfendicAbstract:Regulation of blood glucose homeostasis is complex. Its major hormonal regulators include insulin, glucagon and somatostatin from the endocrine Pancreas. Secretion of these hormones is controlled predominantly by the supply of nutrients in the circulation but also by nerve signals and other peptides. Thus, it is likely that peptides, released from cells of the gut or endocrine Pancreas or from peptidergic nerves, affect glucose homeostasis by modulating the Secretion of insulin, glucagon and somatostatin. When searching for novel gut peptides with such effects, diazepam binding inhibitor (DBI) was isolated from the porcine small intestine. By immunocytochemistry, DBI has been demonstrated to occur not only in the gut but also in endocrine cells of the pancreatic islets, namely in the somatostatin-producing D-cells in pig and man, and in the glucagon-producing A-cells in rat. Porcine DBI (pDBI; 10(-8)-10(-7) M) has been shown to suppress glucose-stimulated release of insulin from both isolated islets and perfused Pancreas of the rat. Furthermore, Secretion of insulin stimulated by either the sulfonylurea glibenclamide or the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), was inhibited by the peptide. In contrast, arginine-induced release of insulin was unaffected by pDBI. Moreover, pDBI decreased arginine-induced release of glucagon from the perfused rat Pancreas, whereas release of somatostatin was unchanged. Notably, rat DBI, structurally identical with rat acyl-CoA-binding protein, has also been demonstrated to inhibit glucose-stimulated release of insulin in the rat, both in vivo and in vitro. Long-term exposure of cultured fetal rat islets to pDBI (10(-8) M) significantly decreased the synthesis of DNA in islet cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Rainer Nustede - One of the best experts on this subject based on the ideXlab platform.
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On the effect of xenin and xenin fragments on exocrine Pancreas Secretion in vivo
Regulatory Peptides, 1999Co-Authors: Rainer Nustede, Wolfgang E Schmidt, O. Horstmann, N. Sikovec, R. Schemminger, Hans Joachim BeckerAbstract:Abstract A stimulatory effect on exocrine Pancreas Secretion could be demonstrated with high concentrations of the 25-amino-acid peptide xenin in non-anesthetized dogs. This peptide has been isolated from gastric mucosa and it is part of a structural coat protein. It has close structural similarities to neurotensin. The longer C-terminal fragments xenin-(13–25) and xenin-(18–25) are essential for the stimulation of exocrine Pancreas Secretion in vivo. The smaller peptide fragments xenin-(21–25) and xenin-(22–25) failed to stimulate the Pancreas as well as the N-terminal peptide fragment xenin-(1–23). The stimulatory effects of xenin may be mediated via neural neurotensin pathways, because neurotensin receptor blockade abolished the stimulatory effect on pancreatic Secretion. Cholinergic pathways are not involved, because atropine had no inhibiting effect.
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Studie zur Regulation der exokrinen Pankreassekretion: Die Bedeutung eines neuen Peptides A study on the regulation of exocrine Pancreas Secretion: The importance of a new peptide
1995Co-Authors: Rainer Nustede, B. Heidrich, K Seyfarth, Wolfgang E Schmidt, Heinz BeckerAbstract:Der Gastrointestinaltrakt verfugt uber ein reichhaltiges System gastrointestinaler Hormone und regulatorischer Peptide. Diese Substanzen sind an der komplexen endokrinen, neuroendokrinen und parakrinen Regulation der Motilitat, der Sekretion und des Gewebswachstums beteiligt. Die diesbezuglich physiologische Bedeutung des neu entdeckten [1] aus 25 Aminosauren bestehenden Peptides Xenin ist noch unbekannt. Erhebliche Mengen des Peptides konnten bisher im humanen Antrum, im Duodenum und im Jejunum ermittelt werden. Es besteht eine strukturelle Verwandtschaft mit Peptiden der sog. Xenopsin-Neurotensin-Familie [2]. Fur das Tridecapeptid Neurotensin konnte bisher eine physiologische Bedeutung fur die endokrine Regulation der exokrinen Pankreassekretion erarbeitet werden [3]. In Anbetracht dieser Zusammenhange sollte daher die Bedeutung des Peptides Xenin fur die Stimulation der exokrinen Pankreassekretion in vivo gepruft werden. Daruber hinaus sollte unter Einsatz des hochspezifischen Neurotensinrezeptorantagonisten SR 4863 2 [ 4] gepruft werden, ob eine peptidinduzierte Wirkung auf das exokrine Pankreas von NeurotensiDrezeptoren vermittelt werden konnte.
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Feedback regulation of exocrine pancreatic Secretion in dogs.
Pancreas, 1993Co-Authors: Anton Schafmayer, Rainer Nustede, Heinz-r. KöhlerAbstract:Important basic physiological mechanisms of exocrine Pancreas Secretion were delineated in a canine model. However, dogs have been considered unsuitable for the study of the controversial feedback regulation of exocrine Pancreas Secretion. The present study reveals a marked modification of Pancreas Secretion following the intraduodenal instillation of lipase: The postprandial lipase Secretion decreases from 2,421 U x 180 min-1 to 1,490 U x 180 min-1, but simultaneously determined cholecystokinin (CCK) concentrations in plasma do not increase under these circumstances. The intraduodenal application of a protease inhibitor (800 mg camostate) significantly stimulates the Secretion of the exocrine Pancreas in the fasting dog: After 15 min the protein release increased to 133 +/- 30 mg. Intravenous atropine blocks this increase. The plasma concentrations of CCK are not significantly influenced. These results in our canine model show that the secretory activity of the exocrine Pancreas depends on the intraduodenal enzyme content. CCK is irrelevant in this context.
A. Karim El-jabali - One of the best experts on this subject based on the ideXlab platform.
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Neural network modeling and control of type 1 diabetes mellitus
Bioprocess and Biosystems Engineering, 2005Co-Authors: A. Karim El-jabaliAbstract:This paper presents a developed and validated dynamic simulation model of type 1 diabetes, that simulates the progression of the disease and the two term controller that is responsible for the insulin released to stabilize the glucose level. The modeling and simulation of type 1 diabetes mellitus is based on an artificial neural network approach. The methodology builds upon an existing rich database on the progression of type 1 diabetes for a group of diabetic patients. The model was found to perform well at estimating the next glucose level over time without control. A neural controller that mimics the Pancreas Secretion of insulin into the body was also developed. This controller is of the two term type: one stage is responsible for short-term and the other for mid-term insulin delivery. It was found that the controller designed predicts an adequate amount of insulin that should be delivered into the body to obtain a normalization of the elevated glucose level. This helps to achieve the main objective of insulin therapy: to obtain an accurate estimate of the amount of insulin to be delivered in order to compensate for the increase in glucose concentration.
Claes-göran Östenson - One of the best experts on this subject based on the ideXlab platform.
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diazepam binding inhibitor and the endocrine Pancreas
Neuropharmacology, 1991Co-Authors: Claes-göran Östenson, Marita Hilliges, Olle Johansson, S Karlsson, Bo Ahrén, Suad EfendicAbstract:Summary Regulation of blood glucose homeostasis is complex. Its major hormonal regulators include insulin, glucagon and somatostatin from the endocrine Pancreas. Secretion of these hormones is controlled predominantly by the supply of nutrients in the circulation but also by nerve signals and other peptides. Thus, it is likely that peptides, released from cells of the gut or endocrine Pancreas or from peptidergic nerves, affect glucose homeostasis by modulating the Secretion of insulin, glucagon and somatostatin. When searching for novel gut peptides with such effects, diazepam binding inhibitor (DBI) was isolated from the porcine small intestine. By immunocytochemistry, DBI has been demonstrated to occur not only in the gut but also in endocrine cells of the pancreatic islets, namely in the somatostatin-producing D-cells in pig and man, and in the glucagon-producing A-cells in rat. Porcine DBI (pDBI; 10 −8 –10 −7 M) has been shown to suppress glucose-stimulated release of insulin from both isolated islets and perfused Pancreas of the rat. Furthermore, Secretion of insulin stimulated by either the sulfonylurea glibenclamide or the phosphodiesterase inhibitor 3-isobutyl-I-methylxanthine (IBMX), was inhibited by the peptide. In contrast, arginine-induced release of insulin was unaffected by pDBI. Moreover, pDBI decreased arginine-induced release of glucagon from the perfused rat Pancreas, whereas release of somatostatin was unchanged. Notably, rat DBI, structurally identical with rat acyl-CoA-binding protein, has also been demonstrated to inhibit glucose-stimulated release of insulin in the rat, both in vivo and in vitro . Long-term exposure of cultured fetal rat islets to pDBI (10 −8 M) significantly decreased the synthesis of DNA in islet cells. In conclusion, DBI moderately suppresses the Secretion of insulin from the B-cells, when stimulated by agents closing ATP-sensitive K + -channels (glucose, glibenclamide) or enhancing the formation of cAMP (IBMX). The mechanism of such an effect is not likely to involve binding of DBI to benzodiazepine-recognition sites of GABA-receptors, since B-cells are reportedly lacking this type of receptor. It cannot be ruled out that the peptide exerts its effect indirectly by binding factors important in regulation of Secretion of insulin, due to its ability to bind amphiphilic compounds. The occurrence of DBI immunoreactivity in non-B-cells of the islets suggests that the peptide may modulate Secretion of insulin locally through paracrine interaction.
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Diazepam binding inhibitor and the endocrine Pancreas.
Neuropharmacology, 1991Co-Authors: Claes-göran Östenson, Marita Hilliges, Olle Johansson, S Karlsson, Bo Ahrén, Suad EfendicAbstract:Regulation of blood glucose homeostasis is complex. Its major hormonal regulators include insulin, glucagon and somatostatin from the endocrine Pancreas. Secretion of these hormones is controlled predominantly by the supply of nutrients in the circulation but also by nerve signals and other peptides. Thus, it is likely that peptides, released from cells of the gut or endocrine Pancreas or from peptidergic nerves, affect glucose homeostasis by modulating the Secretion of insulin, glucagon and somatostatin. When searching for novel gut peptides with such effects, diazepam binding inhibitor (DBI) was isolated from the porcine small intestine. By immunocytochemistry, DBI has been demonstrated to occur not only in the gut but also in endocrine cells of the pancreatic islets, namely in the somatostatin-producing D-cells in pig and man, and in the glucagon-producing A-cells in rat. Porcine DBI (pDBI; 10(-8)-10(-7) M) has been shown to suppress glucose-stimulated release of insulin from both isolated islets and perfused Pancreas of the rat. Furthermore, Secretion of insulin stimulated by either the sulfonylurea glibenclamide or the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), was inhibited by the peptide. In contrast, arginine-induced release of insulin was unaffected by pDBI. Moreover, pDBI decreased arginine-induced release of glucagon from the perfused rat Pancreas, whereas release of somatostatin was unchanged. Notably, rat DBI, structurally identical with rat acyl-CoA-binding protein, has also been demonstrated to inhibit glucose-stimulated release of insulin in the rat, both in vivo and in vitro. Long-term exposure of cultured fetal rat islets to pDBI (10(-8) M) significantly decreased the synthesis of DNA in islet cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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Diazepam binding inhibitor and the endocrine Pancreas.
Neuropharmacology, 1991Co-Authors: Claes-göran Östenson, Marita Hilliges, Olle Johansson, S Karlsson, Bo Ahrén, Suad EfendicAbstract:Regulation of blood glucose homeostasis is complex. Its major hormonal regulators include insulin, glucagon and somatostatin from the endocrine Pancreas. Secretion of these hormones is controlled predominantly by the supply of nutrients in the circulation but also by nerve signals and other peptides. Thus, it is likely that peptides, released from cells of the gut or endocrine Pancreas or from peptidergic nerves, affect glucose homeostasis by modulating the Secretion of insulin, glucagon and somatostatin. When searching for novel gut peptides with such effects, diazepam binding inhibitor (DBI) was isolated from the porcine small intestine. By immunocytochemistry, DBI has been demonstrated to occur not only in the gut but also in endocrine cells of the pancreatic islets, namely in the somatostatin-producing D-cells in pig and man, and in the glucagon-producing A-cells in rat. Porcine DBI (pDBI; 10(-8)-10(-7) M) has been shown to suppress glucose-stimulated release of insulin from both isolated islets and perfused Pancreas of the rat. Furthermore, Secretion of insulin stimulated by either the sulfonylurea glibenclamide or the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), was inhibited by the peptide. In contrast, arginine-induced release of insulin was unaffected by pDBI. Moreover, pDBI decreased arginine-induced release of glucagon from the perfused rat Pancreas, whereas release of somatostatin was unchanged. Notably, rat DBI, structurally identical with rat acyl-CoA-binding protein, has also been demonstrated to inhibit glucose-stimulated release of insulin in the rat, both in vivo and in vitro. Long-term exposure of cultured fetal rat islets to pDBI (10(-8) M) significantly decreased the synthesis of DNA in islet cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Heinz-r. Köhler - One of the best experts on this subject based on the ideXlab platform.
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Feedback regulation of exocrine pancreatic Secretion in dogs.
Pancreas, 1993Co-Authors: Anton Schafmayer, Rainer Nustede, Heinz-r. KöhlerAbstract:Important basic physiological mechanisms of exocrine Pancreas Secretion were delineated in a canine model. However, dogs have been considered unsuitable for the study of the controversial feedback regulation of exocrine Pancreas Secretion. The present study reveals a marked modification of Pancreas Secretion following the intraduodenal instillation of lipase: The postprandial lipase Secretion decreases from 2,421 U x 180 min-1 to 1,490 U x 180 min-1, but simultaneously determined cholecystokinin (CCK) concentrations in plasma do not increase under these circumstances. The intraduodenal application of a protease inhibitor (800 mg camostate) significantly stimulates the Secretion of the exocrine Pancreas in the fasting dog: After 15 min the protein release increased to 133 +/- 30 mg. Intravenous atropine blocks this increase. The plasma concentrations of CCK are not significantly influenced. These results in our canine model show that the secretory activity of the exocrine Pancreas depends on the intraduodenal enzyme content. CCK is irrelevant in this context.
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Influence of extrinsic denervation of the Pancreas on food-stimulated Pancreas Secretion and cholecystokinin and neurotensin release in the dog
Zeitschrift fur Gastroenterologie, 1992Co-Authors: Heinz-r. Köhler, Nustede R, M. Barthel, Anton SchafmayerAbstract:In the present study we examined the effect of extrinsic pancreatic denervation on meal-stimulated pancreatic exocrine Secretion and the release of neurotensin and CCK in dogs. Denervation of the Pancreas significantly decreased protein output from preoperatively 16,661 +/- 1824 mg x 150 min to 2033 +/- 316 mg x 150 min postoperatively (p less than 0.001), and bicarbonate Secretion from 297.5 +/- 36 mmol x 150 min to 104.85 +/- 16 mmol x 150 min (p less than 0.01). Release of neurotensin and CCK was not altered by interruption of the extrinsic pancreatic nerves. Our findings are consistent with the hypothesis that pancreatic secretory response to a meal is predominantly mediated by neutral extrinsic reflexes.
