Chicken Parathyroid Hormone Gene Expression in Response to Gastrin, Omeprazole, Ergocalciferol, and Restricted Food Intake

Persson, Rebecca Gagnemo; Samuelsson, Anna; Håkanson, R.; Persson, Per

doi:10.1007/s002239900325

Cited by 37 publications

(31 citation statements)

References 15 publications

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“…Since the most frequently prescribed calcium supplement is calcium carbonate, which needs a low pH for better absorption, acid blockage with PPIs could pose a problem. In addition, secondary hypergastrinemia due to acid suppression by PPIs may induce hyperparathyroidism and result in increased bone resorption (15,16). The second mechanism focuses on the cells of bone turnover, especially the osteoclasts.…”

Section: Discussionmentioning

confidence: 99%

“…The use of PPIs could increase the risk of bone fractures by affecting calcium homeostasis, which can either be due to inhibition of calcium absorption (13,14) or to the induction of hyperparathyroidism secondary to the development of hypergastrinemia (15,16), although controversy remains. Since PPIs block the acid secretion not only in parietal cells but also in osteoclasts, an essential step in bone resorption (17)(18)(19), they could theoretically decrease the risk of bone fractures and be osteoprotective.…”

Section: Introductionmentioning

confidence: 99%

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Effect of omeprazole on the expression of transcription factors in osteoclasts and osteoblasts

Hyun

Chun²,

Keum³

et al. 2010

Int J Mol Med

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Abstract. The use of proton pump inhibitors (PPIs) seems to be related to increased fracture risk but the mechanism is unclear. In an effort to clarify the mechanism, we evaluated the effect of omeprazole, a representative of the PPIs, on the expression of transcription factors in osteoclasts and osteoblasts. Murine RAW264.7 and MC3T3-E1 cells were used for osteoclast and osteoblast analysis, to which various concentrations of omeprazole were added. RAW264.7 cells with ≥3 nuclei were considered tartrate-resistant acid phosphatase (TRAP)-positive, i.e. activated osteoclasts. Expressions of the calcitonin receptor (CTR), c-fos, nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), and matrix metalloproteinase (MMP)-9 mRNA in osteoclasts were evaluated. Gene expression of osteocalcin and of the osteoprotegerin/receptor activator of NF-κB ligand (OPG/RANKL) ratio in osteoblasts was examined and Western blotting of NFATc1 was performed. Treating the osteoclasts with increasing doses of omeprazole did not affect TRAP positivity, but significantly decreased the expressions of CTR, c-fos, NFATc1, and MMP-9 regardless of the omeprazole concentration. The expression of osteocalcin and of the OPG/RANKL ratio in osteoblasts was augmented with increasing omeprazole concentrations. The result of the Western blot analysis with NFATc1 was similar to that of the expression of NFATc1 mRNA. Omeprazole decreased the activation of osteoclasts but increased that of osteoblasts in vitro, in part causing an osteopetrosis-like effect. Together with the effect of omeprazole on calcium homeostasis, increased fracture risk may be due to the osteopetrorickets-like effect of omeprazole.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of omeprazole on the expression of transcription factors in osteoclasts and osteoblasts

Hyun

Chun²,

Keum³

et al. 2010

Int J Mol Med

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“…A direct effect of gastrin on the parathyroids is unlikely, as gastrin receptors are typically absent from normal and neoplastic parathyroid tissue (28,29). In chickens, hypergastrinaemia induced by administration of omeprazole or infusion of gastrin resulted in increased parathyroid gland weight and PTH gene expression (30). This is in contrast with the findings in fundectomised rats, where hypergastrinaemia had no effect on PTH (31).…”

Section: Discussionmentioning

confidence: 79%

The syndrome of gastric carcinoid and hyperparathyroidism: a family study and literature review

Christopoulos

Balatsos²,

Rotas³

et al. 2009

European Journal of Endocrinology

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Objective: To present evidence supporting the hypothesis that the coexistence of gastric carcinoids (GCs) and hyperparathyroidism may represent a distinct clinical entity, not related to multiple endocrine neoplasia type 1 (MEN1). Methods: We studied a cohort of five young siblings (age range 26-42 years), one of whom had been found to have GC and hyperparathyroidism. All siblings underwent serial gastroscopies for the assessment of gastric neuroendocrine cell proliferations over a mean follow-up period of 31.2 months. Imaging, biochemical and hormonal as well as molecular genetic investigations were performed in the direction of MEN1 syndrome. The literature was searched for cases with coexistence of GCs and hyperparathyroidism not associated with MEN1. Results: Four of the siblings, all male, were found to have GCs in a background of Helicobacter pyloriassociated chronic atrophic gastritis and pernicious anaemia, with no serological evidence of gastric autoimmunity. In two of them, asymptomatic hyperparathyroidism was also present. Screening for MEN1 gene mutations or large deletions was negative, and hormone and imaging investigations did not support a diagnosis of familial MEN1 syndrome. A literature search revealed sporadic reports of cases with GC and hyperparathyroidism not attributable to MEN1. Conclusions: The association of GCs and hyperparathyroidism appears to constitute a distinct syndrome that can be encountered in genetically predisposed individuals, and should not be regarded as 'atypical' or 'incomplete' expression of MEN1. Its prevalence and aetiology should be the subject of future studies. Screening for hyperparathyroidism seems to be justified in patients with GC of any type.

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“…Alternatively, elevated gastrin levels in patients with pernicious anemia could be related to parathyroid hyperfunction, as noted by Selking et al [22], as early as 1982. Although a direct effect of gastrin on the parathyroid glands is unlikely, as gastrin receptors are typically absent from both normal and neoplastic parathyroid tissue [23,24], hypergastrinemia induced by the administration of omeprazole or infusion of gastrin results in increased parathyroid gland weight and PTH gene expression in animal studies [25]. In addition, hypergastrinemia could not be the sole factor predisposing to PTH hypersecretion as shown by the absence of PHP in the fourth control group that included patients with atrophic gastritis and hypergastrinemia, without GC type 1 tumors.…”

Section: Discussionmentioning

confidence: 99%

Primary Hyperparathyroidism in Patients with Gastric Carcinoid Tumors Type 1: An Unusual Coexistence

Thomas

Alexandraki²,

Nikolaou³

et al. 2010

Neuroendocrinology

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Objective: Although a number of familiar syndromes are associated with primary hyperparathyroidism (PHP), there is no information regarding the prevalence of PHP in other sporadic neuroendocrine diseases. The aim of this study is to investigate the prevalence of PHP in our group of patients with gastric carcinoid (GC) type 1 tumors. Methods: Twenty-six patients with biopsy-proven GC type 1 tumors were retrospectively studied. The diagnosis of PHP was suspected following elevated or high-normal serum calcium levels and elevated or inappropriate normal parathyroid hormone levels. Further tests for the localization of the hyperfunctioning parathyroid glands included neck ultrasound, ^99mTc-SESTAMIBI scanning, and cervical or upper mediastinal MR imaging studies. Four control groups were also studied: two age- and sex-matched groups of individuals with (n = 49) and without (n = 34) thyroid autoimmunity and normal endoscopy of the stomach, a third group with nongastric neuroendocrine tumors (n = 68), and a fourth group with atrophic gastritis and hypergastrinemia, without gastric endocrine tumors (n = 30). Results: PHP was diagnosed in 4 (15.38%) patients with GC type 1 tumors compared to none of the 4 control groups. Three of the 4 patients with PHP were operated and proved to have a parathyroid adenoma. No statistically significant differences were observed between patients with or without PHP in mean gastrin and chromogranin A levels, number of lesions, ki-67 labeling index expression, and maximum GC type 1 tumor diameter. Conclusion: PHP seems to be relatively common, approximately 15% in the present cohort, in patients with GC type 1 tumors. PHP should be actively looked for in such patients and treated accordingly.

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Chicken Parathyroid Hormone Gene Expression in Response to Gastrin, Omeprazole, Ergocalciferol, and Restricted Food Intake

Cited by 37 publications

References 15 publications

Effect of omeprazole on the expression of transcription factors in osteoclasts and osteoblasts

Effect of omeprazole on the expression of transcription factors in osteoclasts and osteoblasts

The syndrome of gastric carcinoid and hyperparathyroidism: a family study and literature review

Primary Hyperparathyroidism in Patients with Gastric Carcinoid Tumors Type 1: An Unusual Coexistence

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