Theophylline: Potentiation of Arginine-induced Somatostatin Release from the Isolated Rat Pancreas

Goto, Yasuo; Seino, Yutaka; Taminato, Tomohiko; Kadowaki, Seizo; Chiba, Tsutomu; NOTE, Shinya; Imura, Hiroo

doi:10.2337/diab.28.5.457

Cited by 18 publications

(8 citation statements)

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“…Pancreases and attached segments of duodenum from overnight fasted male Sprague Dawley rats weighing 300-350 g, were perfused in situ by a previously described method [6]. All perfusions were.…”

Section: Methodsmentioning

confidence: 99%

“…Streptozotocin treatment 90 rain prior to the onset of perfusion resulted in changes in somatostatin, glucagon, and insulin responses to glucose and arginine similar to those of alloxan. The present results are consistent with an effect of alloxan and streptozotocin on the D cell similar to that on the B cell, namely, interference with a glucose-mediated effect on hormone secretion.Key words: Alloxan, perfusion, theophylline, streptozotocin, somatostatin, insulin, glucagon, rat, glucose, pancreas, arginine.Somatostatin is localized within the pancreas in secretory granules in D cells of the islets of Langerhans [1, 2] and its secretion is enhanced by glucose [3,4], theophylline [5,6], and glucagon [7]. Administration of exogenous somatostatin inhibits the release of insulin and glucagon [8,9].…”

mentioning

confidence: 99%

“…Somatostatin is localized within the pancreas in secretory granules in D cells of the islets of Langerhans [1, 2] and its secretion is enhanced by glucose [3,4], theophylline [5,6], and glucagon [7]. Administration of exogenous somatostatin inhibits the release of insulin and glucagon [8,9].…”

mentioning

confidence: 99%

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Acute effects of alloxan- and streptozotocin-induced insulin deficiency on somatostatin and glucagon secretion by the perfused isolated rat pancreatico-duodenal preparation

1981

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Summary. The secretion of somatostatin and glucagon by the perfused rat pancreatico-duodenal preparation was examined in situ under control conditions and after the induction of acute insulin deficiency by alloxan or streptozotocin. A 10min 0.625 mmol/1 alloxan perfusion resulted in an immediate and transient increase in basal insulin and glucagon release and a slightly delayed and persistent increase in basal somatostatin secretion. The insulin responses to 16.7mmol/I glucose, 1 mmol/1 theophylline, and 19 mmol/l arginine alone or.in combination were virtually eliminated by atloxan treatment. Somatostatin secretion in response to the stimuli was completely inhibited or markedly attenuated. The glucagon-suppressive effect of glucose was unaltered by alloxan and the stimulatory effect of arginine was enhanced. Addition of 1 ~xg/ml porcine insulin to the perfusion medium did not modify the alterations in somatostatin and glucagon responses to arginine. Streptozotocin treatment 90 rain prior to the onset of perfusion resulted in changes in somatostatin, glucagon, and insulin responses to glucose and arginine similar to those of alloxan. The present results are consistent with an effect of alloxan and streptozotocin on the D cell similar to that on the B cell, namely, interference with a glucose-mediated effect on hormone secretion.Key words: Alloxan, perfusion, theophylline, streptozotocin, somatostatin, insulin, glucagon, rat, glucose, pancreas, arginine.Somatostatin is localized within the pancreas in secretory granules in D cells of the islets of Langerhans [1, 2] and its secretion is enhanced by glucose [3,4], theophylline [5,6], and glucagon [7]. Administration of exogenous somatostatin inhibits the release of insulin and glucagon [8,9]. These observations, together with those of D cell hyperplasia and hypertrophy and of increased pancreatic somatostatin-like immunoreactivity in streptozotocin-and alloxaninduced diabetes in the rat [10][11][12] and in human insulin-dependent diabetes [13], suggest that somatostatin exhibits an important role in the physiology of islet function and possibly in the pathophys.-iology of diabetes.It has recently been reported that plasma somatostatin-like immunoreactivity is elevated in alloxan diabetic dogs [14] and in streptozotocin diabetic rats [15] and that somatostatin secretion from the isolated perfused pancreas of alloxan diabetic rats is exaggerated in response to arginine [16]. In another study, by contrast, normal pancreatic somatostatin responses to arginine, isoproterenol and calcium and a diminished response to glucose were seen in streptozotocin diabetic dogs [17]. The present study was therefore undertaken to investigate further the acute effects of alloxan and streptozotocin on pancreatic somatostatin secretion in the isolated perfused rat pancreas. Materials and MethodsPancreases and attached segments of duodenum from overnight fasted male Sprague Dawley rats weighing 300-350 g, were perfused in situ by a previously described method [6]. All perfusions were. per...

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Section: Methodsmentioning

confidence: 99%

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confidence: 99%

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Acute effects of alloxan- and streptozotocin-induced insulin deficiency on somatostatin and glucagon secretion by the perfused isolated rat pancreatico-duodenal preparation

1981

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“…The release of pancreatic IRS from the isolated perfused rat pancreas [39], rat pancreatic islets [86], and monolayer cell cultures of embryonic chicken pancreas [8], is also aug mented by addition of theophylline to the perfusate or incu bation medium. Theophylline, which results in a rise of cAMP due to inhibition of phosphodiesterase, significantly enhances the stimulatory effects of high glucose levels on insulin and IRS secretion.…”

Section: Effects Of Ca++ and Camp On Somatostatin Release From Gep Ormentioning

confidence: 99%

Somatostatin: Regulation of Secretion

Arimura¹,

Fishback²

1981

Neuroendocrinology

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Somatostatin is released in the blood, in synaptic clefts, and in the intercellular space in response to a variety of stimuli. In view of its multiple functions, various sites of synthesis and release, and rapid inactivation, as well as extremely low levels of somatostatin in the peripheral blood, somatostatin can hardly be considered to be a hormone whose target is reached via the general circulation. The target organs or cells may be located near the somatostatin-producing cells and can be reached via local circulation such as the hypophyseal portal system and the microportal circulation in the gut mucous membrane. Somatostatin released from the neurons acts as a hypophyseotropic hormone and a neurotransmitter or neuromodulator. Furthermore, somatostatin may also act in a paracrine fashion by being released into the intercellular space. This space may sometimes be compartmentalized by tight junctions so that the action of the peptideis limited only to the adjacent cells. In this fashion, the pancreatic islet somatostatin influences nearby A- and B-cell activities. Gut D cells, prototypes of APUD or paraneuron cells, show considerable similarity to neurosecretory cells not only in biochemical processes but also morphologically. While the somatostatin neurons in the brain respond to dopaminergic and catecholaminergic agonists, D cells in the gut respond to chemical stimuli in the lumen by sensing them with microvilli. They release somatostatin into the blood stream, into the intercellular space, and into the gastric and intestinal lumen. Luminal somatostatin may affect other endocrine and nonendocrine cells in the mucous membrane of the gut. It is noted that the same stimulatory agent does not always stimulate somatostatin release from different organs; one agent stimulates the release from one organ and suppresses release from the other organ.

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“…Goto et al (1979) reported that somatostatin, glucagon and insulin release were significantly higher in the presence of 1 mM theophylline with 19 mM arginine than 19 mM arginine only from the isolated rat pancreas.…”

Section: Discussionmentioning

confidence: 96%

Effect of theophylline on insulin, glucagon and somatostation secretion from the isolated rat pancreatico-duodenal preparation.

et al. 1981

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In order to determine whether endogenous somatostatin has an inhibitory action on insulin and glucagon secretion, the isolated rat pancreas was perfused with 10 mM theophylline, which strongly stimulated somatostatin release, under pretreatment or simultaneous administration of 8.3, 16.7 mM glucose and 20 mM arginine with 4.4 mM glucose. 1) In the infusion of 10 mm theophylline with 8.3 mm glucose, the first phase at the time corresponding with that of insulin release elicited by 8.3 mm glucose alone was suppressed by endogenous somatostatin stimulated by theophylline.2) During the infusion of 16.7 mm glucose for 35 min, 10 mM theophylline was interposed at from 15 to 25 min intervals.Its addition caused a rapid increase in somatostatin. Only at 15 min 30 sec and 16 min, insulin concentration went down and reached the levels of 70 and 74 per cent of the 15-min value, respectively. 3) During the infusion of 20 mm arginine with 4.4 mm glucose for 35 min, 10 mM theophylline was added to the perfusate from 15 to 25 min. The addition of theophylline caused an increase in somatostatin and decrease in glucagon. At 15 min 30 sec and 16 min, the levels of glucagon were 63 and 75 per cent of 15-min value, respectively. These results seem to support the idea that endogenous somatostatin suppresses glucose-induced insulin and arginine-induced glucagon secretion. However, the possibility of a direct effect of theophylline on the changes in insulin and glucagon secretion could not be excluded.

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Theophylline: Potentiation of Arginine-induced Somatostatin Release from the Isolated Rat Pancreas

Cited by 18 publications

References 5 publications

Acute effects of alloxan- and streptozotocin-induced insulin deficiency on somatostatin and glucagon secretion by the perfused isolated rat pancreatico-duodenal preparation

Acute effects of alloxan- and streptozotocin-induced insulin deficiency on somatostatin and glucagon secretion by the perfused isolated rat pancreatico-duodenal preparation

Somatostatin: Regulation of Secretion

Effect of theophylline on insulin, glucagon and somatostation secretion from the isolated rat pancreatico-duodenal preparation.

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