Inhibition of Gastrin and Gastric-Acid Secretion by Growth-Hormone Release-Inhibiting Hormone

Bloom, S R; Mortimer, C. H.; Thorner, Michael O.; Besser, G. M.; Hall, R.; Gómez-Pan, A.; Roy, Vikki; Russell, R. C. G.; Coy, David H.; Kastin, A. J.; Schally, Andrew V.

doi:10.1016/s0140-6736(74)90869-1

Cited by 568 publications

(174 citation statements)

References 23 publications

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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: 91%

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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Section: Discussionmentioning

confidence: 91%

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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“…and exerts its physiological actions as a paracrine, endocrine, and neurotransmitter ( 1 ). Its principal effects on the target organ are the inhibition of gastrointestinal hormone functions (2)(3)(4)(5), as well as the inhibition of the secretion of gastrointestinal hormones themselves, such as gastrin, cholecystokinin-pancreozymin (PZ), and secretin (6)(7)(8). Somatostatinoma, which produces somatostatin, is very frequently complicated with cholelithiasis and steatorrhea (9).…”

Section: Introductionmentioning

confidence: 99%

Octreotide Decreases Biliary and Pancreatic Exocrine Function, and Induces Steatorrhea in Healthy Subjects.

et al. 1994

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“…Somatostatin-14 (SST- 14) 4 is a small cyclic peptide hormone secreted by hypothalamus, one of the well known functions of which is to inhibit the release of growth hormone (16). Other important functions of somatostatin-14 include inhibition of gastrin and gastric acid secretion, inhibition of insulin and glucagon secretion in pancreas, and regulation of amyloid-␤ peptide, A␤42, in brain (17)(18)(19) Somatostatin-14 has previously been reported to form amyloid fibrils in vitro (4,20). In this study, we first show that somatostatin-14 is stored as amyloid-like aggregates in rat hypothalamus tissues (Fig.…”

mentioning

confidence: 99%

Elucidating the Role of Disulfide Bond on Amyloid Formation and Fibril Reversibility of Somatostatin-14

Arunagiri

Ranganathan

Dhaked

et al. 2014

Journal of Biological Chemistry

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Background: Peptide/protein hormones are stored as amyloids within endocrine secretory granules. Results: Disulfide bond cleavage enhances conformational dynamics and aggregation kinetics in somatostatin-14, resulting in amyloid fibrils with increased resistance to denaturing conditions and decreased reversibility. Conclusion: Disulfide bond could be a key modulating factor in somatostatin-14 amyloid formation associated with secretory granule biogenesis. Significance: Defective disulfide bonding might cause dysregulation of hormone storage/secretion.

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Inhibition of Gastrin and Gastric-Acid Secretion by Growth-Hormone Release-Inhibiting Hormone

Cited by 568 publications

References 23 publications

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

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

Octreotide Decreases Biliary and Pancreatic Exocrine Function, and Induces Steatorrhea in Healthy Subjects.

Elucidating the Role of Disulfide Bond on Amyloid Formation and Fibril Reversibility of Somatostatin-14

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