GRP-producing nerves control antral somatostatin and gastrin secretion in pigs

Holst, Jens J.; Orskov, C.; Skak‐Nielsen, Tine; Poulsen, Steen Seier; Nielsen, O.B.

doi:10.1152/ajpgi.1987.253.6.g767

Cited by 21 publications

(9 citation statements)

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“…This is different from the reciprocal relationship that normally exists between gastrin and somatostatin in the antrum (Lundell et al 1988, Wu et al 1991. Similar dual increase of these antral peptides is also seen after stimulation with gastrin-releasing polypeptide and administration of glucocorticoids (Holst et al 1987, Xynos et al 1987, Okazaki et al 1993.…”

Section: Introductionmentioning

confidence: 63%

Octreotide inhibits the enterochromaffin-like cell but not peroxisome proliferator-induced hypergastrinemia

Bakke

Sandvik²

2000

Journal of Molecular Endocrinology

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The peroxisome proliferator ciprofibrate induces hypergastrinemia and as a consequence, enterochromaffin-like (ECL) cell hyperplasia. The mechanism for the gastrin cell stimulation is unknown. The somatostatin analog octreotide LAR (long-acting release) was used to see if the stimulating effects of ciprofibrate could be attenuated. Female Fischer rats were dosed with ciprofibrate (50 mg/kg body weight per day) alone or combined with octreotide LAR (10 mg/30 days) for 60 days. Plasma gastrin and histamine, gastric endocrine cell densities and mRNA abundances were measured. Ciprofibrate increased gastrin mRNA abundance (P<0·05), gastrin cell number (P<0·001) and cell area (P<0·01), and induced hypergastrinemia (P<0·001). These rats had profound ECL cell hyperplasia, confirmed by an increase in chromogranin A (CgA) and histidine decarboxylase (HDC) mRNA, density of neuroendocrine and ECL cells and plasma histamine levels (all P<0·001). Octreotide LAR did not affect ciprofibrate stimulation of gastrin cells, but all parameters of ECL cell hyperplasia were reduced (P<0·001). Octreotide LAR also significantly inhibited basal ECL cell function and growth. Ciprofibrate stimulates gastrin cell activity by a mechanism unaffected by octreotide, but octreotide does inhibit basal and gastrin-stimulated ECL cell function and growth.

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Section: Introductionmentioning

confidence: 63%

Octreotide inhibits the enterochromaffin-like cell but not peroxisome proliferator-induced hypergastrinemia

Bakke

Sandvik²

2000

Journal of Molecular Endocrinology

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“…The release of gastrin from the G cell is normally stimulated by proteins in the food (Lichtenberger 1982), and inhibited by gastric acidity (Walsh et al 1975). The vagal nerves also stimulate gastrin release via gastrin releasing peptide (GRP) (Holst et al 1987) whereas somatostatin inhibits gastrin release (Bloom et al 1974). We have previously shown that ciprofibrate, contrary to a previous report (Eason et al 1988a), does not inhibit gastric acid secretion (Martinsen et al 1996).…”

Section: Discussionmentioning

confidence: 90%

The effect of the peroxisome proliferator ciprofibrate on the gastric mucosa and particularly the gastrin cell

Im¹,

Sylte²,

Schulze³

et al. 1998

Journal of Molecular Endocrinology

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The peroxisome proliferator ciprofibrate induces hypergastrinemia without inhibiting acid secretion. The present study was carried out to assess the effect of ciprofibrate on serum gastrin and gastrin (G) cells in different strains of rats and to compare the effect of ciprofibrate with other lipid-reducing agents (lovastatin and simvastatin) which have a different mechanism of action.Serum gastrin was determined by a radioimmunoassay method, G cell density by histomorphometry after immunostaining for G cells, and gastrin, somatostatin and histidine decarboxylase (HDC) mRNA abundance by Northern blot analysis.Ciprofibrate (100 mg/kg/day for three weeks) induced a marked hypergastrinemia (P<0·01) in male and female Fischer rats as well as in female Wistar rats. Simvastatin and lovastatin did not affect serum gastrin. Antral G cell density increased significantly in female Wistar rats (P<0·05) and non-significantly in the other rats after ciprofibrate. Both gastrin and somatostatin mRNA abundance in antral mucosa increased markedly and significantly (P<0·01) after ciprofibrate treatment.The present study shows that the peroxisome proliferator ciprofibrate induces hypergastrinemia secondary to an increased storage and synthesis of antral gastrin. Since somatostatin mRNA abundance also increased, the present study suggests that ciprofibrate and possibly other peroxisome proliferators in sufficient concentrations have a stimulatory effect on endocrine cells.

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“…Fresh Fab fragments were prepared (breach experi ment by a modification of a method described by Mage [22] as previously described in detail [23], Before papain digestion, y-globulins of 2 ml of a potent soma tostatin antiserum (code No. 1756) were precipitated with sodium sulfate.…”

Section: Methodsmentioning

confidence: 99%

Somatostatin Is an Essential Paracrine Link in Acid Inhibition of Gastrin Secretion

Holst¹,

Ørskov²,

Seier-Poulsen³

1992

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We studied the functional coupling between antral somatostatin and gastrin cells in pigs using isolated perfused preparations of the antrum with intact supply of the vagus nerves. Luminal acidification significantly inhibited gastrin secretion to 61 ± 3 % of basal secretion and increased somatostatin output 9-fold. Intra-arterial infusion of somatostatin to concentrations of 10^-10 and 10^-9 mol/l inhibited gastrin secretion to 18 ± 9 and 33 ± 11 % of basal secretion. Electrical stimulation of the vagus nerves and intra-arterial infusion of gastrin-releasing polypeptide (GRP; 10^-9 mol/l) significantly increased both gastrin and somatostatin secretion. Addition to the perfusate of Fab fragments of somatostatin antibodies abolished the effect of somatostatin at 10^-10 mol/l and the acid inhibition of gastrin secretion, but had no effect on the response to vagus stimulation of GRP infusion. We conclude that a local release of somatostatin is essential for the acid-induced inhibition of gastrin secretion, whereas changes in the local somatostatin concentration are unlikely to play a major role in vagally or GRP-induced gastrin secretion.

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GRP-producing nerves control antral somatostatin and gastrin secretion in pigs

Cited by 21 publications

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Octreotide inhibits the enterochromaffin-like cell but not peroxisome proliferator-induced hypergastrinemia

Octreotide inhibits the enterochromaffin-like cell but not peroxisome proliferator-induced hypergastrinemia

The effect of the peroxisome proliferator ciprofibrate on the gastric mucosa and particularly the gastrin cell

Somatostatin Is an Essential Paracrine Link in Acid Inhibition of Gastrin Secretion

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