Adrenergic modulation of insulin and glucagon secretion from the isolated perfused rat pancreas.

Narimiya, Manabu; Yamada, Hideaki; Matsuba, Ikuro; Ikeda, Yoshio; Tanese, Tomio; Abé, Masakazu

doi:10.1507/endocrj1954.28.281

Cited by 15 publications

(1 citation statement)

References 10 publications

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“…There are, however, conflicting results concerning the adrenergic modulation of pancreatic glucagon secretion as to whether the secretion was activated through an a-adrenergic mechanism in dogs (Baum et al 1979), in rabbits (Knudtzon 1984a), in calves Edwards 1978, 1984), in goats (Oda et al 1986) and in sheep (Sasaki et al 1982;Oda et al 1988), or a f3-adrenergic mechanism in human (Atkinson et al 1981), in dogs (Iversen 1973;Boden et al 1982) and in rats (Narimiya et al 1981;Itoh and Gerich 1982) and or both a-and R-adrenergic mechanisms in rats (Nakhooda et al 1981) and in dogs (Samols and Weir 1979).…”

Section: Discussionmentioning

confidence: 99%

.ALPHA.2-Adrenergic modulation of glucagon and insulin secretions in sheep.

Oda

Sasaki

et al. 1991

Tohoku J. Exp. Med.

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To investigate the effects of a2-adrenergic receptors on the secretions of pancreatic glucagon and insulin, clonidine, midaglizole and yohimbine were intravenously administered in four conscious sheep. Clonidine infusion at a dosage of 1.0 nmol/kg/min produced hyperglucagonemia, hypoinsulinemia and hyperglycemia. Midaglizole or yohimbine was infused for 30 min, at doses of 5, 10 and 50 nmol/kg/min during the clonidine infusion. The highest yohimbine infusion (50 nmol/kg/min) blocked the clonidine-induced responses of glucagon, insulin and glucose. On the other hand, the midaglizole (50 nmol/kg/min) infusion brought about no statistical effect on the clonidine-induced responses of glucagon, insulin and glucose. The a2-adrenergic antagonistic effect of midaglizole was clearly less than that of yohimbine in the present experiments. It is concluded that the glucagon secretion is enhanced and the insulin release is inhibited by a2-adrenergic stimulation in conscious sheep.clonidine ; midaglizole ; yohimbine ; glucagon ; insulin Recently, it has been demonstrated that adrenergic subtype receptor mechanism modulates glucagon and insulin secretion in several species. Xylazine, an a2-adrenergic agonist, caused hyperglucagonemia, hypoinsulinemia and hyperglycemia in sheep (Muggaberg and Brockman 1982). Both phenylephrine, an a1-adrenergic agonist, and clonidine, an a2-adrenergic agonist, increased plasma glucagon and lowered plasma insulin in mouse (Skoglund et al. 1987). It has been shown that yohimbine, an a2-adrenergic antagonist, eliminated the glucagon response to epinephrine infusion in rats (Patel 1984), in rabbits (Knudtzon 1984b) and in sheep (Oda et al. 1990). On the contrary, clonidine was ineffective on glucagon secretion in human (Ferlito et al. 1985), in rat islet cell (Schuit and Pipeleers 1986) and in rat pancreas ). Furthermore, studies using metoprolol, a selective /31-adrenergic antagonist, suggest that the adrenergic stimulation of glucagon secretion was mediated through /"1-receptors in rat pancreas ). Thus it may be conceivable that the conflicting results concerning the modulation of glucagon secretion with adrenergic subtype

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Section: Discussionmentioning

confidence: 99%

.ALPHA.2-Adrenergic modulation of glucagon and insulin secretions in sheep.

Oda

Sasaki

et al. 1991

Tohoku J. Exp. Med.

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Effects of isoprenaline and glucagon on insulin secretion from pancreatic islets

Zielmann

Schütte

Lenzen

et al. 1985

Naunyn-Schmiedeberg's Arch. Pharmacol.

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The effects of isoprenaline and glucagon on insulin secretion from pancreatic islets were investigated. In the presence of high concentrations of isoprenaline (10-50 mumol/l), glucose-induced (20 mmol/l) insulin secretion from isolated perifused mouse islets was inhibited. This inhibition was apparently mediated by alpha 2-adrenoceptors, as it was antagonized by rauwolscine. At low concentrations isoprenaline (0.1 or 1 mumol/l) did not affect glucose-induced (2.5; 10 or 20 mmol/l) insulin secretion from perifused mouse or rat islets, even if alpha 2-adrenoceptors were blocked by rauwolscine. A stimulatory effect of isoprenaline on insulin secretion was also not observed in the perfused rat pancreas. However, when incubated mouse islets were exposed to glucose (10 mmol/l), insulin secretion was further enhanced by isoprenaline (0.5 mumol/l). To elucidate the underlying mechanism, the effects of glucagon on insulin secretion were investigated, because glucagon is released from the pancreatic A-cells during stimulation with isoprenaline and is accumulated in the islets and the surrounding medium during incubations of pancreatic islets. Indeed, glucagon stimulated insulin secretion from perifused mouse islets in the presence of high glucose (10 or 15 mmol/l) concentrations but not of low glucose (5 mmol/l) concentrations. Thus it is concluded that direct beta-adrenergic stimulation of pancreatic B-cells does not occur in mouse or rat pancreatic islets. Augmentation of glucose-induced insulin secretion by isoprenaline observed in incubation systems can be explained as a result of stimulation by glucagon, which is released from pancreatic A-cells by isoprenaline.

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