Gastrin and somatostatin in the rat antrum. The effect of removal of acid-secreting mucosa

Lundell, Lars; Bishop, Anne E.; Bloom, S R; Carlsson, Kerstin; Mattsson, Hillevi; Polak, Julia M.; Ryberg, B.

doi:10.1016/0167-0115(88)90423-5

Cited by 9 publications

(9 citation statements)

References 20 publications

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“…However, somatostatin mRNA abundance and area of D cells in group II tended to be increased, and the lack of reduction in D cell parameters accompanying the increase in G cell parameters, is alone in obvious contrast to their normal reciprocal relationship (Lundell et al 1988, Wu et al 1991. The lower dose of ciprofibrate in this study (50 mg/kg body weight) compared with earlier studies (100 mg/kg body weight), may explain the difference in effect on antral D cells.…”

Section: Discussioncontrasting

confidence: 52%

“…Ciprofibrate not only increases gastrin mRNA abundance and raises serum gastrin concentration, but also tends to increase expression of somatostatin in the antrum (Hammer et al 1998. 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: 76%

“…This is consistent with previous studies, showing that ciprofibrate stimulates G cell function and slightly increases G cell density without reducing gastric acidity (Martinsen et al 1996, Hammer et al 1998. Mild G cell hyperplasia caused by sustained achlorhydria has also been reported by others (Lundell et al 1988, Kimura 1993, but further proliferation into G cell carcinoids is rare. Normally somatostatin from the D cells in antrum inhibits G cell function (Saffouri et al 1980, Karnik et al 1989, Zaki et al 1996, and the somatostatin analog octreotide has high affinity for somatostatin receptors of subtype 2 (SSTR-2) located on G cells (Zaki et al 1996).…”

Section: Discussionmentioning

confidence: 97%

“…Apparently, elevated gastric luminal pH due to octreotide suppression of the oxyntic mucosa stimulates G cell function to overcome the direct inhibitory effect of octreotide. Few comparable studies have been done to measure the long-term effects of somatostatin analogs on intragastric pH, but generally previous results indicate that luminal pH and content are dominant regulators of both antral G and D cell functions (Lundell et al 1988, Sandvik & Waldum 1988, Dimaline et al 1991, Wu et al 1991, Kimura 1993, Westbrook et al 1998.…”

Section: Discussionmentioning

confidence: 99%

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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: Discussioncontrasting

confidence: 52%

Section: Introductionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

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

Bakke

Sandvik²

2000

Journal of Molecular Endocrinology

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“…6A), hypochlorhydria is associated with normal or reduced D-cell numbers, often reflecting a physiologic response to sustained elevation of the gastric pH (26,36). Nkx6.3 Ϫ/Ϫ mice differ notably in that D-cell numbers increase in spite of hypogastrinemia and hypochlorhydria.…”

Section: Resultsmentioning

confidence: 99%

Requirement of the Tissue-Restricted Homeodomain Transcription Factor Nkx6.3 in Differentiation of Gastrin-Producing G Cells in the Stomach Antrum

Choi

Romer

Wang

et al. 2008

Molecular and Cellular Biology

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Many homeodomain transcription factors function in organogenesis and cell differentiation. The Nkx family illustrates these functions especially well, and the Nkx6 subfamily controls differentiation in the central nervous system and pancreas. Nkx6.3, a recent addition to this subfamily, overlaps Nkx6.1 and Nkx6.2 in expression in the hindbrain and stomach. Nkx6.3 transcripts localize in the epithelium of the most distal stomach region, the antrum and pylorus; expression in the adult intestine is lower and confined to the proximal duodenum. Nkx6.3 ؊/؊ mice develop and grow normally, with a grossly intact stomach and duodenum. These mice show markedly reduced gastrin mRNA, many fewer gastrin-producing (G) cells in the stomach antrum, hypogastrinemia, and increased stomach luminal pH, with a corresponding increase in somatostatin mRNA levels and antral somatostatin-producing (D) cells. They express normal levels of other transcription factors required for gastric endocrine cell differentiation, Pdx1, Pax6, and Ngn3; conversely, Ngn3 ؊/؊ mice, which also show reduced gastrin levels, express Nkx6.3 normally. These studies implicate Nkx6.3 as a selective regulator of G-and D-cell lineages, which are believed to derive from a common progenitor, and suggest that it operates in parallel with Ngn3.

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Partial gastric corpectomy results in hypergastrinemia and development of gastric enterochromaffinlike-cell carcinoids in the rat

Mattsson¹,

Havu²,

Bräutigam³

et al. 1991

Gastroenterology

119

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Gastrin and somatostatin in the rat antrum. The effect of removal of acid-secreting mucosa

Cited by 9 publications

References 20 publications

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

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

Requirement of the Tissue-Restricted Homeodomain Transcription Factor Nkx6.3 in Differentiation of Gastrin-Producing G Cells in the Stomach Antrum

Partial gastric corpectomy results in hypergastrinemia and development of gastric enterochromaffinlike-cell carcinoids in the rat

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