Effects of glucagon, dibutyryl cyclic 3′,5′-adenosine monophosphate, and theophylline on calcitonin secretion in vitro

Bell, Norman H.

doi:10.1172/jci106353

Cited by 82 publications

(26 citation statements)

References 31 publications

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“…If cAMP and phorbol esters are known to increase CT gene expression [22,23], GLP-1 (7 37) is the first hormonal peptide reported to increase both CGRP and CT mRNAs. At this time, GLP-1 (7-37) is only known as a potent stimulator of insulin secretion in the presence of glucose [6], this effect being mediated by activation of adenylate cyclase and a rise in the intracellular concentration of cAMP [24]. The secretion of GLP-I is stimulated by carbohydrate intake, the absorption of glucose through the sodium/glucose cotransporter stimulates the secretion of GLP-1 [25].…”

Section: Discussionmentioning

confidence: 99%

“…The existence of a gastroentero-thyroidal axis involved in the control of calcitonin (CT) secretion was postulated 23 years ago [5]. Glucagon [6] as well as partially purified enteroglucagon were shown to stimulate the CT secretion rate in pigs [5]. We have therefore studied the effects of GLP-1 (7-37) on the secretion of CGRP and CT by the CA-77 C cell line, and on the steady-state level of their mRNAs.…”

Section: Introductionmentioning

confidence: 99%

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Expression of glucagon‐like peptide 1 receptor in a murine C cell line Regulation of calcitonin gene by glucagon‐like peptide 1

et al. 1996

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We have characterized, by RT-PCR amplification using specific primers, the presence of glucagon-like peptide-I (GLP-I) receptor mRNA in CA-77 cells, a C cell line derived from a rat medullary thyroid carcinoma. Down-regulation of the GLP-1 receptor mRNA was observed after exposure of CA-77 C cells with GLP-1 (7-37). Increased secretion of both calcitonin gene-related peptide (CGRP) and calcitonin (CT) occurred after treatment with GLP-1 (7-37) associated with elevated steadystate levels of CGRP and CT mRNA. GLP-1 (7-37) increased cAMP formation in CA-77 cells in a dose-dependent manner; exendin (9-39), a GLP-1 receptor antagonist, inhibited cAMP production. The GLP-1 peptide which is produced by intestinal cells could be involved in the control of CT secretion through an entero-thyroidal axis implying GLP-1 receptor and increased CT gene expression.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Expression of glucagon‐like peptide 1 receptor in a murine C cell line Regulation of calcitonin gene by glucagon‐like peptide 1

et al. 1996

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“…Secretion of gastrin [6], insulin [3], GH [16], TSH [15], prolactin [20], and prostaglandin [4] were suppressed by the preinfusion of CT. On the other hand, hormone secretions were stimulated by CT infusion in the following hormones, such as ACTH [14], somatostatin [5,10,17], and beta-endorphin [14] secretions. Auto-regulation of CT secretion has been suggested as a feedback mechanism by some researchers using porcine thyroid slices [1,21]. Morimoto et al have supported the presence of a negative feedback mechanism of CT secretion, when salmon CT was administered to rat [19].…”

Section: Introductionmentioning

confidence: 97%

Exogenous Calcitonin Suppresses Growth Fraction of Thyroid C Cells

Mori

Nakamura

Iteya

et al. 2003

Acta Histochem. Cytochem.

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Calcitonin (CT) is a peptide hormone synthesized and secreted by the parafollicular (C) cells of the thyroid. Little is known about the mechanisms controlling proliferation of C cells by other humoral factors including CT, and there is no report that CT suppresses C cell proliferation. The effects of short-term administration of CT on C cell growth fraction were analyzed using BrdU and CT double immunohistochemical method in the rat thyroid. Continuous administration of 0.4 IU/kg and 40 IU/kg synthetic salmon CT for 14 days induced dosedependent suppression of BrdU labeling number of C cells without decrease of C cell to the total thyroid follicular cell ratio. These results suggest that exogenous CT may induce negative feedback to C cell proliferation in the thyroid.

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“…Although calcitonin affects pancreatic function only in pharmacologi cal doses, the physiological relationships with various gastrointestinal hor mones such as glucagon or CCK [3,5] make the as yet unexplained mode of action of this substance a point of interest. In our experiments it was possi ble to demonstrate a significant inhibition of CCK-and secretin-stimulated secretion but not a reduction of basal secretion.…”

Section: Discussionmentioning

confidence: 99%

The Effect of SST, Glucagon, Calcitonin and PGEi on Exocrine Pancreatic Secretion in the Unrestrained Dog in Long-Term Experiments

Funovics¹,

Hölbling²,

Rauhs³

et al. 1981

Eur Surg Res

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Using a new model of a reversible pancreatic fistula which allows the long-term-investigation under nearly physiological conditions on the unrestrained dog, we tested the effect of somatostatin (50 µg), calcitonin (4 µg), glucagon (1 mg), and prostaglan-dine E₁(150 µg) on the exocrine pancreatic function in 45 experiments over a period of 13 h: SST inhibits the basal as well as the secretin or CCK-stimulated secretion: calcitonin shows inhibition of the stimulated secretion only; glucagon blocks the secretin-stimulated pancreatic function; and PGE₁ reduces the bicarbonate concentration and trypsin output in secretin stimulation, but in one of the two series it stimulates the basal secretion.

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Effects of glucagon, dibutyryl cyclic 3′,5′-adenosine monophosphate, and theophylline on calcitonin secretion in vitro

Cited by 82 publications

References 31 publications

Expression of glucagon‐like peptide 1 receptor in a murine C cell line Regulation of calcitonin gene by glucagon‐like peptide 1

Expression of glucagon‐like peptide 1 receptor in a murine C cell line Regulation of calcitonin gene by glucagon‐like peptide 1

Exogenous Calcitonin Suppresses Growth Fraction of Thyroid C Cells

The Effect of SST, Glucagon, Calcitonin and PGEi on Exocrine Pancreatic Secretion in the Unrestrained Dog in Long-Term Experiments

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