Galanin is a potent inhibitor of glucagon-like peptide-1 secretion from rat ileum

Herrmann-Rinke, C.; Hörsch, Dieter; McGregor, G.P.; Göke, Burkhard

doi:10.1016/0196-9781(96)00072-1

Cited by 30 publications

(17 citation statements)

References 32 publications

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“…Considering the presence of galanin immunoreactive nerves throughout the gastrointestinal tract, with galanin fibres projecting into the mucosa (Rattan 1991), our data suggest that the neuropeptide could be a candidate to negatively regulate the postprandial release of GLP-1. This hypothesis is consistent with previous reports that demonstrated an inhibitory effect of galanin on proglucagon-derived peptide secretion (Bauer et al 1989, Herrmann-Rinke et al 1996. Interestingly, galanin also exerts inhibitory effects on pancreatic insulin, glucagon and somatostatin secretions (Hramiak et al 1988, Bauer et al 1989, Amiranoff et al 1990).…”

Section: Discussionsupporting

confidence: 82%

“…Galanin participates in the regulation of intestinal motility and inhibits pancreatic exocrine secretion and insulin release from B-cells (Crawley 1995). It was also shown, in vivo and ex vivo with the isolated vascularly perfused rat ileal model, that galanin reduced the secretory activity of L-cells (Bauer et al 1989, Herrmann-Rinke et al 1996. Since intestinal endocrine cells are under the influence of mediators released from the enteric nervous system, a model of endocrine cells, uncoupled from the underlying lamina propria, is required for further identification of signal transduction pathways put into play by regulatory factors that directly modulate hormone release.…”

Section: Introductionmentioning

confidence: 95%

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Galanin inhibits glucagon-like peptide-1 secretion through pertussis toxin-sensitive G protein and ATP-dependent potassium channels in rat ileal L-cells

Saifia

Chevrier²,

Bosshard³

et al. 1998

Journal of Endocrinology

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The neuropeptide galanin is widely distributed in the gastrointestinal tract and exerts several inhibitory effects, especially on intestinal motility and on insulin release from pancreatic -cells. The presence of galanin fibres not only in the myenteric and submucosal plexus but also in the mucosa, prompted us to investigate the regulatory role of galanin, and its mechanism of action, on the secretion of the insulinotropic hormone glucagon-like peptide-1 (GLP-1). Rat ileal cells were dispersed through mechanical vibration followed by moderate exposure to hyaluronidase, DNase I and EDTA, and enriched for L-cells by counterflow elutriation. A 6-to 7-fold enrichment in GLP-1 cell content was registered after elutriation, as compared with the crude cell preparation (929 81 vs 138 14 fmol/10 6 cells). L-cells then accounted for 4-5% of the total cell population. Bombesin induced a time-(15-240 min) and dose-(0·1 nM-1 µM) dependent release of GLP-1. Glucose-dependent insulinotropic peptide (GIP, 100 nM), forskolin (10 µM) and the phorbol ester 12-0-tetradecanoylphorbol-13-acetate (TPA, 1 µM) each stimulated GLP-1 secretion over a 1-h incubation period. Galanin (0·01-100 nM) induced a dose-dependent inhibition of bombesin-and of GIP-stimulated GLP-1 release (mean inhibition of 90% with 100 nM galanin). Galanin also dose-dependently inhibited forskolininduced GLP-1 secretion (74% of inhibition with 100 nM galanin), but not TPA-stimulated hormone release. Pretreatment of cells with 200 ng/ml pertussis toxin for 3 h, or incubation with the ATP-sensitive K + channel blocker disopyramide (200 µM), prevented the inhibition by galanin of bombesin-and GIP-stimulated GLP-1 secretion. These studies indicate that intestinal secretion of GLP-1 is negatively controlled by galanin, that acts through receptors coupled to pertussis toxin-sensitive G protein and involves ATP-dependent K + channels.

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 95%

Galanin inhibits glucagon-like peptide-1 secretion through pertussis toxin-sensitive G protein and ATP-dependent potassium channels in rat ileal L-cells

Saifia

Chevrier²,

Bosshard³

et al. 1998

Journal of Endocrinology

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“…Galanin is widely expressed in the ENS and, along with somatostatin, is another inhibitor of EEC secretion. In isolated perfused rat ileum, galanin inhibited GIP-stimulated GLP1 release (132); in vitro, galanin inhibited the secretion of several gut hormones including CCK and GLP1 (133,134). These findings are in line with reported effects of galanin in humans, which include a robust inhibition of gastrointestinal motility together with suppression of several gut peptides including PYY and GLP1 but not GIP (135).…”

Section: Gut Microbiota Host Defense and Eec Signalingsupporting

confidence: 80%

Gut chemosensing mechanisms

Psichas¹,

Reimann²,

Gribble³

2015

J. Clin. Invest.

204

176

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“…As mentioned above, several experimental findings have suggested that neural regulation could be of importance, and a variety of neuroactive agents have been shown to influence GLP-1 secretion in previous studies (7,9,19,35). We chose for our studies an experimental model, the isolated perfused porcine ileum, that, judging from a series of previous studies, should be particularly suitable for this purpose.…”

Section: Discussionmentioning

confidence: 99%

“…Infusions of muscarinic cholinergic agonists into isolated perfused rat ileum and colon resulted in stimulation of GLP-1 secretion (9,19,35), and studies in anesthetized rats and in fetal rat intestinal cells suggested that both M1 and M2 muscarinic receptors could be involved in control of GLP-1 release (2). Catecholamines could also be part of a neural stimulatory pathway in rats, as infusion of a ␤-adrenergic agonist stimulated GLP-1 secretion in isolated perfused rat ileum and colon (9, 35).…”

mentioning

confidence: 99%

Neural regulation of glucagon-like peptide-1 secretion in pigs

Hansen

Lampert

Mineo

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

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like peptide (GLP)-1 is secreted rapidly from the intestine postprandially. We therefore investigated its possible neural regulation. With the use of isolated perfused porcine ileum, GLP-1 secretion was measured in response to electrical stimulation of the mixed, perivascular nerve supply and infusions of neuroactive agents alone and in combination with different blocking agents. Electrical nerve stimulation inhibited GLP-1 secretion, an effect abolished by phentolamine. Norepinephrine inhibited secretion, and phentolamine abolished this effect. GLP-1 secretion was stimulated by isoproterenol (abolished by propranolol). Acetylcholine stimulated GLP-1 secretion, and atropine blocked this effect. Dimethylphenylpiperazine stimulated GLP-1 secretion. In chloralose-anesthetized pigs, however, electrical stimulation of the vagal trunks at the level of the diaphragm had no effect on GLP-1 or GLP-2 and weak effects on glucose-dependent insulinotropic peptide and somatostatin secretion, although this elicited a marked atropine-resistant release of the neuropeptide vasoactive intestinal polypeptide to the portal circulation. Thus GLP-1 secretion is inhibited by the sympathetic nerves to the gut and may be stimulated by intrinsic cholinergic nerves, whereas the extrinsic vagal supply has no effect. somatostatin; nerve stimulation; enteric nervous system; vasoactive intestinal polypeptide; incretin hormones GLUCAGON-LIKE PEPTIDE (GLP)-1 is a peptide primarily produced in the lower part of the gut (reviewed in Ref. 22). It is known as an incretin hormone (stimulating insulin secretion) (27) and thought to be part of the "ileal brake" mechanism (inhibition of upper gut motility and secretion elicited by the presences of unabsorbed nutrients in the ileum) (28,32,44). Thus infusions of GLP-1 have been shown to reduce appetite and energy intake in humans (14). Relatively little is known about the mechanisms that regulate GLP-1 secretion in pigs and humans.The presence of unabsorbed nutrients in the lumen seems to be an important stimulus for GLP-1 secretion in rats (38), pigs (23), and humans (28). However, the response to a meal is usually rapid, with increases in the plasma concentration occurring within a few minutes after the start of meal ingestion (6,10,24,34,38), before the bulk of the meal is thought to have reached the lower gut. This suggests that a neural and/or an endocrine pathway from the upper part of the gastrointestinal tract to the lower gut may exist.In rats, glucose-dependent insulinotropic peptide (GIP) has been shown to stimulate GLP-1 secretion (9,20,35,38), although recent studies have indicated that a neural pathway involving the vagus nerve (2, 39) might predominate compared with a direct endocrine pathway. Infusions of muscarinic cholinergic agonists into isolated perfused rat ileum and colon resulted in stimulation of GLP-1 secretion (9,19,35), and studies in anesthetized rats and in fetal rat intestinal cells suggested that both M1 and M2 muscarinic receptors could be involved in control of GLP-1 rel...

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Galanin is a potent inhibitor of glucagon-like peptide-1 secretion from rat ileum

Cited by 30 publications

References 32 publications

Galanin inhibits glucagon-like peptide-1 secretion through pertussis toxin-sensitive G protein and ATP-dependent potassium channels in rat ileal L-cells

Galanin inhibits glucagon-like peptide-1 secretion through pertussis toxin-sensitive G protein and ATP-dependent potassium channels in rat ileal L-cells

Gut chemosensing mechanisms

Neural regulation of glucagon-like peptide-1 secretion in pigs

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