Insulin release by glucagon and secretin: studies with secretin-glucagon hybrids

Kofod, Hans; Andreu, David; Thams, Peter; Merrifield, R. B.; Hedeskov, C. J.; Hansen, Birgit Sehested; Lernmark, Åke

doi:10.1152/ajpendo.1988.254.4.e454

Cited by 7 publications

(1 citation statement)

References 8 publications

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“…Sct was shown to specifically augment glucose-stimulated insulin release as it did not change the insulin responses to arginine, isoproterenol, tolbutamide and glucagon [59]. In mouse pancreatic islets cells, Sct potentiated in-vitro glucose-stimulated insulin release [51] and the N-terminal region of the peptide was shown to be important for this effect [50]. In rats, Sct stimulates insulin secretion without increasing the blood flow to the islets [14], but simultaneously, several reports negate such insulinotropic effects.…”

Section: Secretin and Insulin/glucose Homeostasismentioning

confidence: 97%

Metabolic effects of secretin

Sekar

Chow

2013

General and Comparative Endocrinology

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Secretin (Sct), traditionally a gastrointestinal hormone backed by a century long research, is now beginning to be recognized also as a neuroactive peptide. Substantiation by recent evidence on the functional role of Sct in various regions of the brain, especially on its potential neurosecretion from the posterior pituitary, has revealed Sct's physiological actions in regulating water homeostasis. Recent advances in understanding the functional roles of central and peripheral Sct has been made possible by the development of Sct and Sct receptor (SctR) knockout animal models which have led to novel approaches in research on the physiology of this brain-gut peptide. While research on the role of Sct in appetite regulation and fatty acid metabolism has been initiated recently, its role in glucose homeostasis is unclear. This review focuses mainly on the metabolic role of Sct by discussing data from the last century and recent discoveries, with emphasis on the need for revisiting and elucidating the role of Sct in metabolism and energy homeostasis.

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Section: Secretin and Insulin/glucose Homeostasismentioning

confidence: 97%

Metabolic effects of secretin

Sekar

Chow

2013

General and Comparative Endocrinology

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Characterization of the G protein coupling of a glucagon receptor to the KATP channel in insulin-secreting cells

Ribalet

Ciani

1994

J. Membarin Biol.

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The G-protein-mediated coupling of a glucagon receptor to ATP-dependent K channels--KATP--has been studied in insulin-secreting cells using the patch clamp technique. In excised outside-out patches, KATP channel activity was inhibited by low concentrations of glucagon (IC50 = 2.4 nM); the inhibitory effect vanished at concentrations greater than 50 nM. In cell-attached patches, inhibition by bath-applied glucagon was seen most often, although stimulation was observed in a few cases. A dual action of the hormone is proposed to resolve these apparently divergent results. In excised inside-out patches, KATP channel activity was inhibited by addition of beta gamma subunits purified from either erythrocyte or retina (IC50 = 50 pM and 1 nM, respectively). Subsequent exposure of the patch to alpha i or alpha o reversed this effect. In excised inside-out patches, increasing Mg2+ in the bath stimulated the channel activity between 0 and 0.5 nM, but blocked it at higher concentrations (IC50 = 2.55 mM). In most cases (70%), GTP had a stimulatory effect at concentrations up to 100 microns. However, in three cases, similar GTP levels had clear inhibitory effects. In excised inside-out patches, cholera toxin (CTX) caused channel inhibition. Although the effect could not be reversed by removal of the toxin, the activity was restored by subsequent addition of purified alpha i or alpha o. These results are compatible with a model whereby channel inhibition by activated Gs-coupled receptors occurs, at least in part, via association of the beta gamma subunits of Gs with alpha i/alpha o subunits and deactivation of the alpha i/alpha o-dependent stimulatory pathway. On the basis of this hypothesis, a model is developed to describe the effects of G proteins on the KATP channel, as well as to account for the concentration-dependent stimulation and inhibition of KATP channel by Mg2+. An interpretation of the ability of glucagon to potentiate, but not initiate, insulin release is also given in terms of this model and the effects of ATP on KATP channels.

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Effect of C-terminal fragments of glucagon on insulin secretion in dogs

Ohneda

1994

Metabolism

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Insulin release by glucagon and secretin: studies with secretin-glucagon hybrids

Cited by 7 publications

References 8 publications

Metabolic effects of secretin

Metabolic effects of secretin

Characterization of the G protein coupling of a glucagon receptor to the KATP channel in insulin-secreting cells

Effect of C-terminal fragments of glucagon on insulin secretion in dogs

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