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Papers by Rebecca Gagnemo Persson
Scandinavian Journal of Gastroenterology, 1996
Gastrin stimulates uptake of Ca(2)+ into bone and causes transient hypocalcemia, possibly by rele... more Gastrin stimulates uptake of Ca(2)+ into bone and causes transient hypocalcemia, possibly by releasing a peptide hormone from enterochromaffin-like (ECL) cells, which are histamine- and peptidehormone-producing cells in the acid-producing part of the stomach. However, if ECL cells secrete a calciotropic hormone, it is to be expected that their activity is affected by the serum Ca(2)+ concentration. Food-deprived male rats were infused with human (Leu)15-gastrin-17 and/or ethylenediamine-tetraacetic acid and CaCl(2). The blood Ca(2)+ level was monitored throughout the experiments (3 h), and the serum concentrations of gastrin, parathyroid hormone, and calcitonin were measured at death. The activity of the ECL cells was assessed by measuring the histidine decarboxylase (HDC) activity. Gastrin produced the expected increase in HDC activity, but neither hyper- nor hypo-calcemia affected the RDC activity of either hypo- or hyper-gastrinemic rats. Perturbations in blood Ca(2)+ do not seem to affect ECL cells, which is at odds with the view that ECL cells harbor a calciotropic hormone.
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Endocrinology, 1991
As in the rat, gastrin and an extract of the acid-producing part of the stomach (proventriculus) ... more As in the rat, gastrin and an extract of the acid-producing part of the stomach (proventriculus) were found to lower the blood Ca2+ concentration in the chicken. Furthermore, gastrin enhanced the uptake of 45Ca into the femur. It has been suggested previously that gastrin causes hypocalcemia in the rat by releasing gastrocalcin, a hypothetical hormone thought to reside in the acid-producing part of the stomach. The results of the present study in the chicken are in agreement with this concept. Not only exogenous, but also endogenous gastrin lowered blood calcium levels. Thus, the serum gastrin concentration was increased in response to ranitidine-evoked blockade of the gastric acid output; the rise in gastrin was associated with a transient drop in blood calcium. Also, food intake produced a rise in the serum gastrin concentration and a transient drop in blood calcium. However, injection of ranitidine or food intake in proventriclectomized (acid-producing part of the stomach extirpated) chickens failed to lower blood calcium, supporting the view that the gastrin-evoked hypocalcemia depends upon an agent in the gastric (proventriculus) mucosa. We suggest that endogenous and exogenous gastrin evoke hypocalcemia in the chicken by the same mechanism as that which has been postulated in the rat, i.e. by mobilization of the candidate hormone gastrocalcin from endocrine cells in the acid-producing gastric mucosa.
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Calcified Tissue International, 1997
Treatment with omeprazole, a long-acting proton pump inhibitor of acid secretion, induces hyperga... more Treatment with omeprazole, a long-acting proton pump inhibitor of acid secretion, induces hypergastrinemia. In chickens, omeprazole induces growth not only of the acid-producing mucosa (probably reflecting the trophic action of gastrin), but also of the parathyroid glands (hypertrophy + hyperplasia), while suppressing bone density and body weight gain without affecting blood calcium. The first part of the present study was concerned with the effect of omeprazole, ergocalciferol (vitamin D2), and restricted food intake on the gene expression of parathyroid hormone (PTH) in the parathyroid glands of the chicken. Chickens were treated with omeprazole (400 μmol/kg/day, I.M.), food restriction, omeprazole + food restriction, ergocalciferol (250 000 IU/kg/day, S.C.), or ergocalciferol + omeprazole for 5 weeks. The weight gain of the chickens was monitored, and the weights of the parathyroid glands and femurs were determined at sacrifice. PTH mRNA in the parathyroid glands was analyzed by Northern blot. The second part of the study examined the effect of 3 weeks of continuous gastrin infusion (chicken gastrin 20–36, 5 nmol/kg/hour, S.C.) on the expression of PTH mRNA in the parathyroid glands. Omeprazole reduced the body weight and femur density (ash weight per volume) while greatly increasing the weight of the parathyroid glands and the PTH gene expression. Food restriction alone and ergocalciferol alone (at a dose that raised blood Ca2+) were without effect, but food restriction greatly enhanced the omeprazole-evoked increase in parathyroid gland weight and PTH gene expression. Gastrin increased the weight of the parathyroid glands and reproduced the effect of omeprazole on PTH gene expression. Hence, it seems likely that the effect of omeprazole reflects the ensuing hypergastrinemia.
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Regulatory Peptides, 2002
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Biochemical and Biophysical Research Communications, 2000
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Scandinavian Journal of Gastroenterology, 1994
Omeprazole, a long-acting inhibitor of gastric acid secretion, is able to increase the circulatin... more Omeprazole, a long-acting inhibitor of gastric acid secretion, is able to increase the circulating concentrations of gastrin. Daily treatment with high doses of omeprazole cause sustained hypergastrinemia. Long-standing hypergastrinemia can be expected to exert numerous effects in the body. For instance, gastrin has been proposed to promote growth in the digestive tract and pancreas. The present study is concerned with the effect of omeprazole on parathyroid glands in the chicken. Chickens were treated with omeprazole (400 mumol/kg/day) in methylcellulose (2.5 ml/kg) for 5 or 10 weeks. Controls received vehicle. Blood calcium and serum gastrin concentrations were studied. The weight gain of the animals and of various organs (proventriculus, antrum, thyroids, parathyroids, ultimobranchial glands, and femur) were determined. The DNA content and the size of the parathyroid chief cells were also determined. Omeprazole reduced the body weight gain while greatly increasing the weight of the proventriculus and the parathyroid glands. The weight and density of the femur were reduced. The circulating concentrations of calcium were unaffected. The DNA content of the parathyroid glands was increased, and morphometric analysis of the parathyroid chief cells showed an increased cell size. Thus, the increased parathyroid gland weight seems to reflect both hypertrophy and hyperplasia. There was a slight increase in the weight of the ultimobranchial glands (expressed per kilogram body weight). The weight of the thyroids was unaffected (expressed in relation to body weight). The results indicate that omeprazole treatment in chickens leads not only to trophic effects in the acid-producing gastric mucosa (probably because of the ensuing hypergastrinemia), as reported earlier, but also to growth of the parathyroid glands (both hypertrophy and hyperplasia) and to bone loss without affecting blood calcium values. The mechanism behind these effects remains unknown.
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Pharmacology & Toxicology, 2001
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Gut, 1991
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Calcified Tissue International, 1993
Young male rats (100 g body weight) were fed diets containing varying amounts of calcium. Body we... more Young male rats (100 g body weight) were fed diets containing varying amounts of calcium. Body weight and bone development were studied together with various endocrine parameters, including blood levels of Ca2+, calcitonin, parathyroid hormone, vitamin D, and gastrin, and the enterochromaffin-like (ECL) cell-related parameters gastric mucosal histidine decarboxylase activity and histamine concentration. A diet containing 0.5% calcium resulted in ontimum body weight gain and bone development. A lower calcium intake impaired body weight gain and bone development. The impairment was manifested in reduced bone calcium content whereas the size of the bones was unaffected. The net absorption of calcium seemed to be proportional to the calcium intake. A low calcium diet (0.03%) raised the circulating levels of 1,25(OH)2D and parathyroid hormone and lowered 25(OH)D3 and Ca2+, whereas a high calcium diet (5.46%) raised calcitonin, Ca2+, 25(OH)D3, and 1,25(OH)2D. In addition, the low calcium diet lowered the circulating gastrin concentation and the histidine decarboxylase activity and histamine content of the ECL cells in the gastric mucosa. A high calcium diet raised the circulating gastrin concentration, but the rise was not associated with an increase in the histidine decarboxylase activity and histamine content.
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Regulatory Peptides, 1999
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Scandinavian Journal of Gastroenterology, 1996
Gastrin stimulates uptake of Ca(2)+ into bone and causes transient hypocalcemia, possibly by rele... more Gastrin stimulates uptake of Ca(2)+ into bone and causes transient hypocalcemia, possibly by releasing a peptide hormone from enterochromaffin-like (ECL) cells, which are histamine- and peptidehormone-producing cells in the acid-producing part of the stomach. However, if ECL cells secrete a calciotropic hormone, it is to be expected that their activity is affected by the serum Ca(2)+ concentration. Food-deprived male rats were infused with human (Leu)15-gastrin-17 and/or ethylenediamine-tetraacetic acid and CaCl(2). The blood Ca(2)+ level was monitored throughout the experiments (3 h), and the serum concentrations of gastrin, parathyroid hormone, and calcitonin were measured at death. The activity of the ECL cells was assessed by measuring the histidine decarboxylase (HDC) activity. Gastrin produced the expected increase in HDC activity, but neither hyper- nor hypo-calcemia affected the RDC activity of either hypo- or hyper-gastrinemic rats. Perturbations in blood Ca(2)+ do not seem to affect ECL cells, which is at odds with the view that ECL cells harbor a calciotropic hormone.
Bookmarks Related papers MentionsView impact
Endocrinology, 1991
As in the rat, gastrin and an extract of the acid-producing part of the stomach (proventriculus) ... more As in the rat, gastrin and an extract of the acid-producing part of the stomach (proventriculus) were found to lower the blood Ca2+ concentration in the chicken. Furthermore, gastrin enhanced the uptake of 45Ca into the femur. It has been suggested previously that gastrin causes hypocalcemia in the rat by releasing gastrocalcin, a hypothetical hormone thought to reside in the acid-producing part of the stomach. The results of the present study in the chicken are in agreement with this concept. Not only exogenous, but also endogenous gastrin lowered blood calcium levels. Thus, the serum gastrin concentration was increased in response to ranitidine-evoked blockade of the gastric acid output; the rise in gastrin was associated with a transient drop in blood calcium. Also, food intake produced a rise in the serum gastrin concentration and a transient drop in blood calcium. However, injection of ranitidine or food intake in proventriclectomized (acid-producing part of the stomach extirpated) chickens failed to lower blood calcium, supporting the view that the gastrin-evoked hypocalcemia depends upon an agent in the gastric (proventriculus) mucosa. We suggest that endogenous and exogenous gastrin evoke hypocalcemia in the chicken by the same mechanism as that which has been postulated in the rat, i.e. by mobilization of the candidate hormone gastrocalcin from endocrine cells in the acid-producing gastric mucosa.
Bookmarks Related papers MentionsView impact
Calcified Tissue International, 1997
Treatment with omeprazole, a long-acting proton pump inhibitor of acid secretion, induces hyperga... more Treatment with omeprazole, a long-acting proton pump inhibitor of acid secretion, induces hypergastrinemia. In chickens, omeprazole induces growth not only of the acid-producing mucosa (probably reflecting the trophic action of gastrin), but also of the parathyroid glands (hypertrophy + hyperplasia), while suppressing bone density and body weight gain without affecting blood calcium. The first part of the present study was concerned with the effect of omeprazole, ergocalciferol (vitamin D2), and restricted food intake on the gene expression of parathyroid hormone (PTH) in the parathyroid glands of the chicken. Chickens were treated with omeprazole (400 μmol/kg/day, I.M.), food restriction, omeprazole + food restriction, ergocalciferol (250 000 IU/kg/day, S.C.), or ergocalciferol + omeprazole for 5 weeks. The weight gain of the chickens was monitored, and the weights of the parathyroid glands and femurs were determined at sacrifice. PTH mRNA in the parathyroid glands was analyzed by Northern blot. The second part of the study examined the effect of 3 weeks of continuous gastrin infusion (chicken gastrin 20–36, 5 nmol/kg/hour, S.C.) on the expression of PTH mRNA in the parathyroid glands. Omeprazole reduced the body weight and femur density (ash weight per volume) while greatly increasing the weight of the parathyroid glands and the PTH gene expression. Food restriction alone and ergocalciferol alone (at a dose that raised blood Ca2+) were without effect, but food restriction greatly enhanced the omeprazole-evoked increase in parathyroid gland weight and PTH gene expression. Gastrin increased the weight of the parathyroid glands and reproduced the effect of omeprazole on PTH gene expression. Hence, it seems likely that the effect of omeprazole reflects the ensuing hypergastrinemia.
Bookmarks Related papers MentionsView impact
Regulatory Peptides, 2002
Bookmarks Related papers MentionsView impact
Biochemical and Biophysical Research Communications, 2000
Bookmarks Related papers MentionsView impact
Scandinavian Journal of Gastroenterology, 1994
Omeprazole, a long-acting inhibitor of gastric acid secretion, is able to increase the circulatin... more Omeprazole, a long-acting inhibitor of gastric acid secretion, is able to increase the circulating concentrations of gastrin. Daily treatment with high doses of omeprazole cause sustained hypergastrinemia. Long-standing hypergastrinemia can be expected to exert numerous effects in the body. For instance, gastrin has been proposed to promote growth in the digestive tract and pancreas. The present study is concerned with the effect of omeprazole on parathyroid glands in the chicken. Chickens were treated with omeprazole (400 mumol/kg/day) in methylcellulose (2.5 ml/kg) for 5 or 10 weeks. Controls received vehicle. Blood calcium and serum gastrin concentrations were studied. The weight gain of the animals and of various organs (proventriculus, antrum, thyroids, parathyroids, ultimobranchial glands, and femur) were determined. The DNA content and the size of the parathyroid chief cells were also determined. Omeprazole reduced the body weight gain while greatly increasing the weight of the proventriculus and the parathyroid glands. The weight and density of the femur were reduced. The circulating concentrations of calcium were unaffected. The DNA content of the parathyroid glands was increased, and morphometric analysis of the parathyroid chief cells showed an increased cell size. Thus, the increased parathyroid gland weight seems to reflect both hypertrophy and hyperplasia. There was a slight increase in the weight of the ultimobranchial glands (expressed per kilogram body weight). The weight of the thyroids was unaffected (expressed in relation to body weight). The results indicate that omeprazole treatment in chickens leads not only to trophic effects in the acid-producing gastric mucosa (probably because of the ensuing hypergastrinemia), as reported earlier, but also to growth of the parathyroid glands (both hypertrophy and hyperplasia) and to bone loss without affecting blood calcium values. The mechanism behind these effects remains unknown.
Bookmarks Related papers MentionsView impact
Pharmacology & Toxicology, 2001
Bookmarks Related papers MentionsView impact
Gut, 1991
Bookmarks Related papers MentionsView impact
Calcified Tissue International, 1993
Young male rats (100 g body weight) were fed diets containing varying amounts of calcium. Body we... more Young male rats (100 g body weight) were fed diets containing varying amounts of calcium. Body weight and bone development were studied together with various endocrine parameters, including blood levels of Ca2+, calcitonin, parathyroid hormone, vitamin D, and gastrin, and the enterochromaffin-like (ECL) cell-related parameters gastric mucosal histidine decarboxylase activity and histamine concentration. A diet containing 0.5% calcium resulted in ontimum body weight gain and bone development. A lower calcium intake impaired body weight gain and bone development. The impairment was manifested in reduced bone calcium content whereas the size of the bones was unaffected. The net absorption of calcium seemed to be proportional to the calcium intake. A low calcium diet (0.03%) raised the circulating levels of 1,25(OH)2D and parathyroid hormone and lowered 25(OH)D3 and Ca2+, whereas a high calcium diet (5.46%) raised calcitonin, Ca2+, 25(OH)D3, and 1,25(OH)2D. In addition, the low calcium diet lowered the circulating gastrin concentation and the histidine decarboxylase activity and histamine content of the ECL cells in the gastric mucosa. A high calcium diet raised the circulating gastrin concentration, but the rise was not associated with an increase in the histidine decarboxylase activity and histamine content.
Bookmarks Related papers MentionsView impact
Regulatory Peptides, 1999
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