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PubMed1983

Zinc-induced hypocalcemia and bone resorption in rats.

The changes of calcium levels in serum and in the femur were examined in rats administered oral doses of zinc sulfate (0.1, 1.0, and 10 mg Zn/100 g body weight) for 3 days. All doses of zinc caused significant decreases in calcium levels in serum and in the femoral diaphysis and epiphysis. The decrease in these femoral calcium levels was seen 1 day after administration of zinc (10 mg/100 g). Furthermore, time course studies of the effect of zinc administration showed that, at 1 hr after zinc administration, calcium levels in serum and in femoral epiphysis but not in diaphysis were significantly decreased. In thyroparathyroidectomized rats, however, no significant decrease of the epiphyseal calcium was observed by administration of zinc (10 mg Zn/100 g), but the serum calcium level was significantly lowered. Zinc administration to intact rats caused a significant increase in acid phosphatase activity in the femoral epiphysis but not in the diaphysis. This increase was clearly prevented by thyroparathyroidectomy. Accumulations of zinc in the femoral epiphysis and diaphysis after zinc administration was not significantly altered by thyroparathyroidectomy. These results suggest that zinc-induced hypocalcemia may cause bone resorption which is primarily mediated by the action of the parathyroid hormone and it is related to calcium homeostasis in rats.

Acid Phosphatase↗

PubMed1981

Renal phosphate adaptation in uraemic dogs with a remnant kidney.

1. Clearance and micropuncture studies were performed in 27 dogs made uraemic by segmental infarction to examine the factors responsible for phosphate adaptation in chronic renal failure. 2. The animals were studied before and after extracellular volume expansion to 10% of body weight in the presence and absence of parathyroid glands. The results were compared with 19 normal dogs studied under similar experimental conditions. 3. In the dogs with a remnant kidney and intact parathyroids adaptation of phosphate transport was evident, with a high fractional excretion of phosphate. Thyroparathyroidectomy 3 days before study in the dogs with a remnant kidney and moderate renal failure reduced fractional excretion of phosphate to near normal values, indicating a major role of parathyroid hormone in phosphate adaptation. Extracellular volume expansion in these thyroparathyroidectomized uraemic dogs led to an exaggerated phosphaturic response with fractional excretion of phosphate returning towards the value in the uraemic dogs with intact parathyroid glands. Thus acute extracellular volume expansion could also contribute to the increase in fractional phosphate excretion, but extracellular volume probably plays a relative minor role in the adaptation of phosphate excretion. 4. With more advanced renal failure fractional excretion of phosphate remained high, even after thyroparathyroidectomized, indicating that parathyroid hormone-independent factors become important for phosphate adaptation in the advanced stage of renal failure. The nature of parathyroid hormone-independent changes in fractional phosphate reabsorption in chronic renal failure remains unknown. 5. Proximal tubular fluid/plasma ultrafiltrate phosphate ratios were high in all groups of dogs with a remnant kidney regardless of thyroparathyroidectomy or the degree of renal failure. The non-specific nature of the proximal tubule pattern of phosphate transport indicates that phosphate adaptation is primarily determined by alterations in phosphate transport at a site distal to the proximal convoluted tubule. Alternatively, deep nephrons may play a greater role in determination of the overall phosphate adaptation in the chronically diseased kidney.

Adaptation, Physiological↗

PubMed1992

Effects of parathyroid hormone and calcium and their interrelationship on urinary acidification in the rat.

1. The influence of thyroparathyroidectomy on renal function and specifically on acid excretion was studied in rats with or without oral supplementation of calcium. 2. Thyroparathyroidectomy caused a significant decrease in glomerular filtration rate, in the urinary/plasma inulin ratio and in overall acid excretion. These changes were not corrected by calcium supplementation. 3. Rates of proximal tubular acidification were studied by means of double-barrelled resin/reference microelectrodes. Acidification half-time was significantly increased in both thyroparathyroidectomized and calcium-supplemented thyroparathyroidectomized rats (8.38 s and 7.40 s, respectively) compared with control rats (5.44 s). 4. When 10(-6) mol/l A23187, a calcium ionophore, was added to the luminal bicarbonate solution, the acidification half-time returned to 3.97 s in the thyroparathyroidectomized rats, whereas no significant changes were detected in the properties of acidification in the control rats. 5. These data show that parathyroid hormone and cellular calcium are important factors involved in proximal tubular H+ secretion, which appears to be largely dependent on a well-defined concentration range of these agents.

Animals↗

PubMed1980

Diurnal changes in calcium and phosphate metabolism in rats.

Diurnal changes in the metabolism of calcium and phosphate were studied in fasted conscious rats by use of a perfusion balance study method. On a light dark 12:12 h schedule and on a constant iv load of calcium among other nutrients, the animals exhibited a diurnal rhythm in which urinary excretion of calcium was low in the night and high in the day. This was accompanied by a reciprocal change in phosphate balance (high excretion in the night, and low in the day). The diurnal change was abolished by adrenalectomy. Thyroparathyroidectomy alone did not prevent the diurnal change. It was abolished, however, when thyroparathyroidectomy was followed by a constant infusion of parathyroid hormone (0.8 U/h). These data indicate the presence of a diurnal rhythm of calcium and phosphate metabolism in rats and the involvement of parathyroid and adrenal hormones in the genesis of the rhythms.

Animals↗

PubMed1972

Control of 25-hydroxycholecalciferol metabolism by parathyroid glands.

Thyroparathyroidectomy of rats on a diet low in calcium reduces production of 1,25-dihydroxycholecalciferol from 25-hydroxycholecalciferol to negligible levels within 40 hr, and increases production of another metabolite, called Va. Parathyroid extract, at a dose of 20 units per day, prevents these changes. When 40 units per day of parathyroid extract is given 48 hr after thyroparathyroidectomy, 1,25-dihydroxycholecalciferol production is restored almost to control levels within 36 hr. The change brought about by parathyroid extract cannot be attributed to resulting changes in serum calcium or phosphorus concentration. It appears that the parathyroid hormone serves as a tropin for production of 1,25-dihydroxycholecalciferol, the hormonal form of vitamin D responsible for calcium mobilization from intestinal contents and bone.

Animals↗

PubMed1981

Measurement of mammalian 25-hydroxyvitamin D3 24R-and 1 alpha-hydroxylase.

An in vitro assay of mammalian 25-hydroxyvitamin D3 1 alpha- and 24R-hydroxylases in kidney has been developed. It had been suggested that 25-hydroxyvitamin D binding protein present in mammalian blood and tissues inhibits the enzyme activities in cell-free preparations by binding the substrate 25-hydroxyvitamin D3 more strongly than the hydroxylases bind it. This inhibitory effect is overcome by the addition of substantial amounts of unlabeled 25-hydroxyvitamin D3 to saturate the binding sites of this protein. The resulting metabolites produced in vitro by rat kidney homogenates were isolated and firmly identified by ultraviolet absorption spectrometry and mass spectrometry as 1,25-dihydroxyvitamin D3 and (24R)-24,25-dihydroxyvitamin D3. Maximal 1 alpha-hydroxylation of 25-hydroxyvitamin D3 could be demonstrated in kidney homogenates prepared from vitamin D-deficient rats. Thyroparathyroidectomy of these rats resulted in total suppression of the 1 alpha-hydroxylase. Homogenates of kidney from rats given vitamin D showed little or no 1 alpha-hydroxylase and substantial 24R-hydroxylase activity. Thyroparathyroidectomy of these rts markedly increased the 24R-hydroxylase activity.

24,25-Dihydroxyvitamin D 3↗

PubMed1984

Rat renal 25-hydroxyvitamin D3 1- and 24-hydroxylases: their in vivo regulation.

The effects of thyroparathyroidectomy, parathyroid hormone, 1,25-dihydroxyvitamin D3, dietary calcium, dietary phosphorus, age, and sex on the renal 25-hydroxyvitamin D3 1- and 24-hydroxylases measured in vitro in rats have been studied. Thyroparathyroidectomy of vitamin D-deficient rats abolishes 25-hydroxyvitamin D3 1-hydroxylase activity, and administration of bovine parathyroid extract to the thyroparathyroidectomized rat restores diminished 1-hydroxylase activity. Both suppression and restoration of the enzyme activities require many hours (18-24 h) independent of rapid changes in serum calcium and inorganic phosphorus levels in response to these manipulations. Administration of 1,25-dihydroxyvitamin D3 to vitamin D-deficient rats suppresses 25-hydroxyvitamin D3 1-hydroxylase activity and stimulates 25-hydroxyvitamin D3 24-hydroxylase activity within 48 h. Rats maintained on a low-calcium or a low-phosphorus diet with a daily supplement of 20 IU vitamin D3 show high 25-hydroxyvitamin D3 1-hydroxylase activity and low 24-hydroxylase activity as compared with rats similarly treated but fed a diet containing adequate calcium or adequate phosphorus. When vitamin D-sufficient rats having suppressed renal 25-hydroxyvitamin D3 1-hydroxylase activity are placed on a low-calcium vitamin D-deficient diet for 7 days, the 1-hydroxylase activity is greatly stimulated in 6-wk-old rats but much less so in rats with advancing age.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

PubMed1984

Relationship of antral gastrin cells and serum gastrin to thyroid function in the rat.

Using a quantitative immunocytochemical technique, antral gastrin cell populations in the rat were studied in various states of thyroid function. Simultaneous determinations of circulating serum gastrin were made by RIA. Rats made hypothyroid by ingestion of methimazole (0.01% solution in drinking water for 30 days) demonstrated a significant 32% decrease in gastrin cell density (306 +/- 9/cm vs. 207 +/- 11/cm for controls) associated with a significant 50% decrease in serum gastrin (143 +/- 12 vs. 307 +/- 20 pg/ml for controls). Induction of hypothyroidism and hypoparathyroidism by surgical thyroparathyroidectomy resulted in similarly significant decreases in gastrin cell numbers (229 +/- 12/cm) and serum gastrin (169 +/- 14 pg/ml). Animals that underwent thyroparathyroidectomy followed by T4 replacement (2.5 micrograms/100 g X day, ip) for 30 days had a mean gastrin cell density that was not significantly different from that of controls; serum gastrin was decreased to 207 +/- 11 pg/ml. The administration of excess T4 (200 micrograms/100 g X day, ip) for either 15 or 30 days was associated with a significant increase in gastrin cell numbers (413 +/- 23/cm at 15 days; 352 +/- 21/cm at 30 days). Mean serum gastrin was increased by 82% after 15 days of T4 administration (558 +/- 51 pg/ml) and by 65% at 30 days (506 +/- 36 pg/ml). We conclude that T4 is trophic for gastrin cells in the rat.

Animals↗

PubMed1992

Somatic gene transfer in the development of an animal model for primary hyperparathyroidism.

The overproduction of hormones is associated with a variety of endocrinological disorders. We have used somatic cell gene transfer of human PTH (hPTH) to develop an animal model of hypercalcemia and osteoclastic skeletal resorption. Recombinant retroviruses were used to transduce a functional hPTH gene into cultured rat fibroblasts. The recombinant-derived preproparathyroid hormone peptide was appropriately processed in this ectopic cell, and intact hPTH (1-84) was secreted at a high level (2-5 ng/10(6) cells/24 h). Transplantation of the PTH-secreting cells into syngeneic rat recipients was associated with the development of hypercalcemia mediated by increasing serum concentrations of hPTH. Thyroparathyroidectomy in these hypercalcemic rats producing hPTH did not result in hypocalcemia and tetany, which was observed in control animals undergoing thyroparathyroidectomy. Chronic overproduction of hPTH (60 days) was associated with severe hypercalcemia, metastatic calcification, and histological changes of osteoclastic resorption of bone. This animal model will be useful in studying the pathophysiology of severe hyperparathyroidism in humans and should help in the evaluation of new medical therapies for hypercalcemia.

3T3 Cells↗

PubMed1996

Antibody to beta3 integrin inhibits osteoclast-mediated bone resorption in the thyroparathyroidectomized rat.

The cell surface integrin, alphaVbeta3, is important for the attachment of osteoclasts to bone matrix and the subsequent resorption of bone. The present study was designed to determine the effects of F11, a monoclonal antibody to the rat beta3 subunit, on calcium mobilization in a rat model of bone resorption. Male Sprague Dawley rats became hypocalcemic within 18 h after thyroparathyroidectomy. Synthetic PTH-related protein (PTHrP(1-34)) administered to control rats caused serum calcium to return to normal. Anti-beta3 treatment of rats after thyroparathyroidectomy inhibited the calcemic response to PTHrP by 65%. Circulating F11 was biologically active as demonstrated by osteoclast retraction and by the inhibition of adenosine diphosphate-induced platelet aggregation via inhibition of the platelet integrin alphaIIbbeta3 in ex vivo assays. F11 antibody was localized by immunohistological staining to osteoclasts in long bones, suggesting that the mechanism of action of the antibody was via a direct effect upon osteoclasts. Echistatin and calcitonin also inhibited calcemic responses to PTHrP in this in vivo model, whereas an isotype-matched, control antibody was ineffective. These studies provide the first direct evidence in vivo that osteoclast-mediated bone resorption is regulated via beta3 integrin.

Animals↗

PubMed1980

Pentagastrin and glucagon stimulate serum somatostatin-like immunoreactivity in man.

Passive immunization with somatostatin (SRIF) antiserum suggests that gastrin, glucagon, and calcitonin secretion may be exerted either locally by contiguity of SRIF-like immunoreactivity (SRIF-LI)-containing D cells and G (gastrin) and A (glucagon) cells (paracrine) or by an endocrine effect. To determine whether a reciprocal relationship exists in man between these peptides and SRIF-LI, the effects of pentagastrin (0.5 microgram/kg BW), glucagon (1 mg), and calcium (15 mg/kg BW) on serum SRIF-LI were examined. The coexistence of SRIF-LI and calcitonin in normal thyroid parafollicular C cells and medullary carcinoma of the thyroid prompted a study of the effects of the known secretagogues of calcitonin, calcium (15 mg/kg BW), and pentagastrin (0.5 microgram/kg BW) on serum SRIF-LI. Sixteen normal subjects, two patients with metastatic medullary carcinoma of the thyroid, and one patient who had undergone thyroparathyroidectomy were evaluated. We demonstrated that whereas both pentagastrin and glucagon significantly elevated serum SRIF-LI, calcium infusion had no effect. Basal and stimulated SRIF-LI levels in the normal controls, patients with medullary carcinoma of the thyroid, and the patient with thyroparathyroidectomy were similar. These results suggest that SRIF-LI secretion is related to stimulation by peptides produced in closely juxtaposed cells, that SRIF-LI, unlike calcitonin, may not be a serum marker for medullary carcinoma of the thyroid in man, and that little, if any, serum SRIF-LI originates in the thyroid.

Calcitonin↗

PubMed1990

Depression of calcium pump activity in renal cortex of vitamin D-deficient rats with secondary hyperparathyroidism.

To examine the hormonal regulation of the ATP-dependent Ca2+ pump in the kidneys, the ATP-dependent Ca2+ uptake by the basolateral membrane vesicles in the renal cortex was measured using radioactive calcium (45Ca2+) in rats with vitamin D deficiency or rats undergoing thyroparathyroidectomy. The Vmax of the Ca2+ pump activity was increased not only by administering calcitriol, but also by normalizing the serum calcium level in vitamin D-deficient rats. PTH suppressed the Ca2+ pump activity in normocalcemic vitamin D-deficient rats. Thyroparathyroidectomy did not affect the Ca2+ pump activity in the kidneys of normal rats. It was concluded that the ATP-dependent Ca2+ pump activity was depressed by secondary hyperparathyroidism in vitamin D-deficient rats.

Adenosine Triphosphate↗

PubMed1992

The significance of the gastroprotective effect of body protection compound (BPC): modulation by different procedures.

To elucidate any mechanism of a body protecting effect the observed events should be investigated also by the way of their modulations induced by ablation of particular organs. For Body Protection Compound (BPC), a newly partially characterized gastric juice peptide, the gastroprotection has largely been studied in basal and modified conditions of 48 h-restraint stress. Ablations or sham operations have been performed before restraint as follows: 60 min vagotomy, 24 h ovaria, testes, spleen, 48 h medulla of adrenal glands, 40 days thyroid + parathyroid glands. BPC (10 micrograms/kg) or saline (5 ml/kg) have been regularly applied (after surgery, 1 h before restraint) intraperitoneally. The group subjected to thyroparathyroidectomy received also once-daily BPC/saline treatment. A very strong gastroprotective effect in basal conditions has been modulated by ovariectomy and demedullation (abolishment), thyroparathyroidectomy (decrease), and no change occurred in case of vagotomy, splenectomy or orchidectomy. Sham operated rats did not differ from corresponding controls. Thus, seeing from point of view a wide range of organoprotective effects of BPC (intestinum, kidney, liver, pancreas, inflammation, diabetes mellitus, delayed type of hypersensitivity), the gastroprotection has been supposed a) to be of crucial pattern in the general concept of organo-protection and b) to be responsible for the mediation of the suggested "stomach stress organoprotective response". Therefore, the obtained modulations suggest a complex and specifical, sex-related action of the overall beneficial effects of BPC.

Adrenalectomy↗

PubMed1983

Effects of metabolic alkalosis on calcium excretion in the conscious dog.

The tubular reabsorption of calcium has been studied in chronic metabolic alkalosis and acidosis. Clearance studies were performed in five conscious mongrel dogs during control periods and during alkalosis and acidosis both before and after thyroparathyroidectomy. After thyroparathyroidectomy, normocalcemia was maintained with oral dihydrotachysterol, and thyroxine was replaced. An initial control study was followed by the induction of chronic metabolic alkalosis by repeated gastric drainage for 4 days through a previously implanted gastric fistula. A second control study 1 week after alkalosis was followed by the induction of acidosis by feeding ammonium chloride, 10 gm daily for 3 days. A final control study was performed 1 week later. Serum proteins, GFR, and filtered calcium load were not significantly different in control, alkalosis, or acidosis. Alkalosis, in both intact and TPTX dogs, was associated with no change in TRNa in comparison with controls (94.6% vs. 95.4 in intact, p greater than 0.05; 95.0% vs. 96.3% in TPTX, p greater than 0.05). By contrast, TRCa increased significantly (97.2% vs. 95.5, p less than 0.05 in intact; 98.0% vs. 95.0, p less than 0.05 in TPTX). In acidosis, TRNa in both intact and TPTX dogs was unchanged in comparison with control (96.4%, p greater than 0.05 and 96.6%, p greater than 0.05, respectively), and TRCa was significantly decreased (to 91.9%, p less than 0.01 and 83.3%, p less than 0.001, respectively). These data indicate that chronic metabolic alkalosis increases the TRCa independently of changes in TRNa, filtered calcium load, or parathyroid activity.

Acidosis↗

PubMed1981

[Influence of thyroid states on PGE2 biosynthesis].

Hyperthyroid and hypothyroid states were induced in the rat by daily injection of 3,3',5-triiodothyronine (T3; 33 microgram/100 g b. wt., ip for 6 days) or by thyroparathyroidectomy, respectively. Control animals underwent only a sham operation or received the T3 vehicle. In these experimental conditions the biosynthesis of PGE2-like substance was determined "in vitro" in the fraction obtained after centrifugation at 80,000xg for 60 min of pooled spleens (5). Assays of PGE2 activity were carried out on rat stomach strip preparations according to Vane (8). In a series of additional experiments the influence of thyroid states on the inhibitory activity exerted by Indomethacin, Oxametacine and Phenylbutazone on PGE2 biosynthesis was also evaluated. The results obtained indicate that the hyperthyroidism induces a significant increase of PGE2 production "in vitro" from added arachidonic acid (100% enhancement above the control values) while thyroparathyroidectomy is unable to interfere with such biosynthetic activity. In addition, the inhibitory effect of Indomethacin, Oxametacine and Phenylbutazone on PGE2 production is not affected by hyperthyroid state whereas hypothyroidism significantly limits the action of the mentioned non-steroid anti-inflammatory agents.

Animals↗

PubMed1982

Atrophy of the zona fasciculata in the adrenal cortex of thyroparathyroidectomized rats: a quantitative study.

Atrophy of the adrenal gland induced by thyroparathyroidectomy (TPX) is attributable primarily to narrowing of the zona fasciculata. But absolute volumes of the adrenal gland and zona fasciculata, not the zona glomerulosa and zona reticularis, were decreased significantly 7 weeks after TPX. Changes consistent with atrophy were also seen in the zona fasciculata by electron microscopy. A slight decrease in volume of cytoplasm in cells of the zona fasciculata was evident 2 weeks after TPX as shown by quantitative stereological techniques. Seven weeks after TPX, there was a significant decrease in average cytoplasmic volume as well as mitochondrial volume and surface density of mitochondrial membranes. A decrease in total volume of the zona fasciculata, as well as volume per cell of mitochondria, correlates directly with decreased production of corticosterone in response to stress in TPX rats. Parathyroidectomy (PX) had no effect on the volume of the adrenal gland, on the volume of the individual cortical zones, or on the volume per cell of cytoplasm or mitochondria; these observations indicate that changes in TPX rats are due primarily to ablation of the thyroid gland.

Adrenal Cortex↗

PubMed1994

Evaluation of urinary pyridinium crosslink excretion as a marker of bone resorption in the rat.

The aim of this study was to evaluate the value of the urinary excretion of the pyridinium crosslinks, pyridinoline (Pyr) and deoxypyridinoline (D-Pyr), as markers of bone resorption in the rat. The excretion of the crosslinks was compared with that of urinary [3H]tetracycline ([3H]TC) excretion from chronically [3H]TC-prelabeled animals, a technique established to monitor bone resorption in the rat. Bone resorption was modulated by Ca restriction, infusion of PTH, thyroparathyroidectomy, and administration of different bisphosphonates. Furthermore, the urinary crosslinks were assessed in three different osteopetrotic mutations in the rat. We found a delayed response of Pyr and D-Pyr excretion to acute changes in bone resorption compared with [3H]TC excretion. This delay was 1 day after Ca restriction and longer after other treatments, such as PTH administration or bisphosphonate treatment, with which it was more than 3 weeks. In contrast, chronic states with stimulation or inhibition of bone resorption showed similar changes in excretion of the urinary crosslinks and [3H]TC, except after PTH administration. The excretion of the crosslinks was greatly reduced in osteopetrotic rats (op/op, tl/tl, and ia/ia) and increased to normal levels in tl/tl rats after stimulation of bone resorption by M-CSF administration. These results suggest that, in rats, urinary excretion of the pyridinium crosslinks reflects bone resorption in chronic but not always in acute conditions. The cause of this discrepancy is still unclear.

Amino Acids↗

PubMed1978

Polyamine metabolism in regenerating livers from normal and hypocalcemic rats.

There is a marked increase in the concentration of putrescine during the first ten hours following partial hepatectomy in rats. The concentration of spermidine also increases but to a smaller degree. Putrescine levels return to normal between 10 and 24 hours after the operation, whereas the increased spermidine level is maintained. The production of putrescine and spermidine appears to be initiated by the induction of ornithine decarboxylase which shows a single peak of activity at four hours after hepatectomy. The activity of S-adenosylmethionine decarboxylase shows little change following hepatectomy. The changes in polyamine levels and the activities of the enzymes of polyamine metabolism are not affected by thyroparathyroidectomy 72 hours prior to hepatectomy. Thus although these hypocalcemic conditions considerably reduce and delay DNA synthesis and mitosis, the prereplicative changes in polyamine metabolism still occur. These data suggest that the hepatocytes in hypocalcemic animals have become activated and moved to an advanced stage of prereplicative development before being blocked.

Adenosylmethionine Decarboxylase↗