Effect of 1,25-dihydroxyvitamin D3 on plasma concentrations of calcium-binding protein in normal and rachitic (vitamin D-dependent rickets type I) pigs

1987 ◽  
Vol 115 (1) ◽  
pp. 129-134
Author(s):  
E. M. W. Maunder ◽  
A. V. Pillay ◽  
A. D. Care
Keyword(s):  
Vitamin D ◽  
Plasma Concentration ◽  
Calcium Binding ◽  
Binding Protein ◽  
Plasma Concentrations ◽  
Calcium Binding Protein ◽  
Type I ◽  
Dihydroxyvitamin D3 ◽  
Calbindin D ◽  
Permissive Role

ABSTRACT An i.v. injection of calcitriol (1,25-(OH)2D3) had no effect within 2·5 h on plasma concentrations of calbindin-D9k (vitamin D-induced calcium-binding protein; CaBP) in hypocalcaemic pigs with inherited vitamin D-dependent rickets type I or in their normocalcaemic siblings or half-siblings. Three days later the plasma concentration of CaBP had doubled in the hypocalcaemic pigs, but was unaltered in the normocalcaemic siblings and half-siblings. Following daily i.v. injections of 1,25-(OH)2D3 for a further 5 days (days 4–8) plasma concentrations of CaBP increased in both the hypocalcaemic (days 4–8) and normocalcaemic (day 8) pigs, the effect being more rapid and greater in the hypocalcaemic 1,25-(OH)2D3-deficient animals. An i.v. injection of 1,25-(OH)2D3 to pure Yucatan pigs also had no effect on plasma concentrations of CaBP within 1·5 h, but in the following 1 h there was some indication of an increase in plasma CaBP levels. In contrast to the normal pigs, insulin-induced hypoglycaemia did not lead to a peak in plasma CaBP concentrations in the hypocalcaemic pigs. There was also no change in the plasma concentrations of 1,25-(OH)2D3 associated with the peak in plasma CaBP following insulin-induced hypoglycaemia in normocalcaemic pigs. These results suggest that changes in plasma concentrations of 1,25-(OH)2D3 are not directly involved in mediating the increase in plasma CaBP which follows hypoglycaemia induced by insulin in normal pigs, although 1,25-(OH)2D3 probably plays a permissive role. J. Endocr. (1987) 115, 129–134

Endocrine control of plasma concentrations of calcium-binding protein in the pig

1987 ◽  
Vol 115 (1) ◽  
pp. 121-128
Author(s):  
E. M. W. Maunder ◽  
A. V. Pillay ◽  
A. D. Care
Keyword(s):  
Calcium Binding ◽  
Binding Protein ◽  
Plasma Concentrations ◽  
Significant Rise ◽  
Calcium Binding Protein ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Endocrine Control ◽  
Adrenergic Blocker ◽  
Calbindin D

ABSTRACT The aetiology of the rise in plasma calbindin-D9k (vitamin D-induced calcium-binding protein; CaBP), following insulin-induced hypoglycaemia, was studied in the pig. ACTH led to a rise in plasma concentrations of both CaBP and cortisol. Metyrapone, which blocks cortisol synthesis, abolished the increases in plasma concentrations of CaBP and cortisol normally observed in response to insulin-induced hypoglycaemia. However, there was no significant rise in plasma concentrations of CaBP in response to pharmacological or physiological doses of cortisol. Injection of clonidine, an α2-adrenergic agonist, led to a rise in plasma concentrations of CaBP, whereas phenylephrine, an α1-adrenergic agonist, tended to exert an inhibitory effect. Also, administration of phentolamine (an α-adrenergic blocker) before injection of insulin abolished the usual increase in plasma concentrations of CaBP, whereas propranolol (a β-adrenergic blocker) enhanced the normal increase in plasma concentrations of CaBP in response to insulin-induced hypoglycaemia. Isoproterenol, a β-adrenergic agonist, was without effect on plasma CaBP. Neither GH nor glucagon appear to be involved in the rise in plasma CaBP following insulin-induced hypoglycaemia. Although atropine abolished the effect of acute hypoglycaemia on plasma CaBP, carbamylcholine was without effect on plasma CaBP concentration. It is concluded that the increases in plasma CaBP induced by either ACTH or α2-adrenergic stimulation may be interrelated since the administration of ACTH can lead to raised plasma concentrations of catecholamines. J. Endocr. (1987) 115, 121–128

Raised levels of calcium-binding protein in plasma following insulin-induced hypoglycaemia in the pig

1986 ◽  
Vol 109 (1) ◽  
pp. 101-106 ◽  
Author(s):  
E. M. W. Maunder ◽  
A. V. Pillay ◽  
C. Chapman ◽  
A. D. Care
Keyword(s):  
Vitamin D ◽  
Calcium Binding ◽  
Inorganic Phosphate ◽  
Binding Protein ◽  
Plasma Concentrations ◽  
Calcium Binding Protein ◽  
Insulin Administration ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Normal Calcium

ABSTRACT Insulin-induced hypoglycaemia in the pig elicited sharp increases in the plasma concentrations of vitamin D-dependent calcium-binding protein (CaBP) and cortisol and a decrease in plasma inorganic phosphate. Glucose infusion following insulin administration abolished the increases in plasma CaBP and cortisol in response to insulin and reduced the hypophosphataemia. The percentage increases in plasma CaBP and cortisol in response to insulin-induced hypoglycaemia were reduced when the pigs were fed a low-calcium diet, but the hypophosphataemic response was similar. We conclude that insulin-induced hypoglycaemia leads to increased plasma CaBP in pigs fed a normal calcium diet, which is associated with the hypoglycaemia rather than being a direct effect of insulin. We therefore suggest that plasma CaBP may represent more than a mere uncontrolled leak from its sites of storage. J. Endocr. (1986) 109, 101–106

Intestinal vitamin D-induced calcium-binding protein: time-course of immunocytological localization following 1,25-dihydroxyvitamin D3.

1983 ◽  
Vol 31 (3) ◽  
pp. 426-432 ◽  
Author(s):  
A N Taylor
Keyword(s):  
Vitamin D ◽  
Calcium Binding ◽  
Calcium Transport ◽  
Time Course ◽  
Binding Protein ◽  
Calcium Binding Protein ◽  
Dihydroxyvitamin D3 ◽  
Migration Rates ◽  
1,25 Dihydroxyvitamin D3 ◽  
Free Cells

The vitamin D-induced calcium-binding protein (CaBP) was localized in histological sections of chick duodenum using the peroxidase-antiperoxidase immunocytochemical technique. The time-course of appearance of CaBP in rachitic chicks was investigated from 0 to 120 hr after stimulation by 1,25-dihydroxyvitamin D3 (1,25(OH)2D3). CaBP was not routinely detected at 0 hr after 1,25(OH)2D3 administration. CaBP was first noted in some, but not all, of the samples taken 2 hr following 1,25(OH)2D3 and was detected in all 2 1/2 hr samples. The number of CaBP-containing absorptive cells and the apparent CaBP concentration both increased to a maximum at about 16-24 hr. At later times, as CaBP free cells migrated up the villi, the CaBP-containing cells decreased in number, but even at 120 hr post 1,25(OH)2D3 dose there were significant numbers of CaBP-containing cells present. The relationships between time-course of CaBP location on intestinal villi, enterocyte migration rates, and the time-course of 1,25(OH)2D3 stimulated intestinal calcium transport are discussed.

Sign in / Sign up

Export Citation Format

Share Document