The Role of Parathyroid Hormone in the Gastro-Intestinal Absorption of Calcium

1970 ◽  
Vol 39 (1) ◽  
pp. 89-94 ◽  
Author(s):  
M. R. Wills ◽  
J. Wortsman ◽  
C. Y. C. Pak ◽  
F. C. Bartter

1. Gastrointestinal calcium absorption was studied in six normal subjects and in one patient with idiopathic hypoparathyroidism during a control period and during treatment with parathyroid extract. 2. In all subjects there was a small increase in the gastro-intestinal absorption of calcium during the administration of parathyroid extract.

1982 ◽  
Vol 94 (3) ◽  
pp. 443-453 ◽  
Author(s):  
C. J. Robinson ◽  
E. Spanos ◽  
M. F. James ◽  
J. W. Pike ◽  
M. R. Haussler ◽  
...  

Intestinal calcium absorption and plasma levels of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) were measured in lactating and non-lactating rats and the effects of bromocriptine and exogenous prolactin treatment were evaluated. In lactating rats calcium absorption and plasma levels of parathyroid hormone, 1,25(OH)2D3 and alkaline phosphatase activity were significantly increased. Bromocriptine treatment significantly reduced the enhanced calcium absorption and levels of plasma 1,25(OH)2D3 and alkaline phosphatase but had no significant effect on plasma levels of parathyroid hormone. Prolactin administered with bromocriptine to lactating animals prevented all the changes observed with bromocriptine treatment alone. It was concluded that the increased plasma levels of prolactin during lactation lead to high plasma levels of 1,25(OH)2D3 which are responsible for the enhanced intestinal calcium absorption.


1972 ◽  
Vol 55 (2) ◽  
pp. 245-252 ◽  
Author(s):  
D. N. KALU ◽  
CARMEL HILLYARD ◽  
G. V. FOSTER

SUMMARY The effect of glucagon on bone was studied in rats. Urinary hydroxyproline excretion and incorporation of [3H]proline into bone hydroxyproline were used as indices of bone collagen breakdown and formation respectively. Parathyroid extract (15 USP units/rat/h, i.v.), infused into thyroparathyroidectomized animals, increased urinary hydroxyproline excretion. This increase was nullified by simultaneous administration of glucagon (50 μg/rat/h, i.v.). Rats treated with glucagon for 12 days (30 μg/100 g/day, s.c.) excreted slightly less hydroxyproline in their urine than controls. In both intact and thyroparathyroidectomized rats, glucagon (10 μg/100 g/h, s.c.) decreased incorporation of [3H]proline into bone. Similar results were obtained in nephrectomized rats, evidence that changes produced by glucagon were not solely due to alterations in proline pool size caused by increased renal excretion. From these data it is concluded that: (1) glucagon can inhibit bone resorption (the effect being slight in normal rats, but easily demonstrable in parathyroid hormone-treated thyroparathyroidectomized rats), (2) release of endogenous calcitonin is not required to produce this effect, (3) parathyroid hormone and glucagon may act on the same target cell in bone, (4) inhibition of skeletal resorption may contribute to glucagon-induced hypocalcaemia, and (5) the hormone possibly decreases bone formation. Since pharmacological doses of glucagon were used in our studies, the relationship of the observations made to the physiological role of glucagon is unknown.


1990 ◽  
Vol 258 (2) ◽  
pp. E263-E268 ◽  
Author(s):  
J. K. Yeh ◽  
J. F. Aloia

The response of calciotropic hormones and bone turnover to exercise and immobilization was examined by the measurement of calcium balance, bone turnover indexes, levels of parathyroid hormone, nephrogenous adenosine 3',5'-cyclic monophosphate (cAMP), and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] weekly for 6 wk in three groups of rats: control, exercise trained, and immobilized. Early in the experiment, increases were observed in excretion of urinary calcium, hydroxyproline, and in serum alkaline phosphatase after both exercise and immobilization. It was not until the latter part of the experimental period that changes were observed in nephrogenous cAMP and intestinal absorption efficiency of calcium. In the fasting state, the exercise group had a drop in serum calcium and phosphate and a rise in nephrogenous cAMP and serum 1,25(OH)2D3 compared with the control group. The exercised animals experienced an increase in bone mass, whereas the immobilized animals had a decline in bone mass. Thus exercise stimulates bone growth, resulting in an increased demand for minerals that is satisfied by an increase in serum 1,25(OH)2D3 levels and increased intestinal absorption of calcium. The increase in calcium absorption suppresses parathyroid hormone production (nephrogenous cAMP) in the exercised animal. Immobilization resulted in increased bone resorption that suppressed parathyroid hormone, nephrogenous cAMP, and the intestinal absorption of calcium.


1973 ◽  
Vol 73 (3) ◽  
pp. 489-498 ◽  
Author(s):  
R. Hehrmann ◽  
J. Hagemann ◽  
R. Montz ◽  
E. Jentsch

ABSTRACT The effects of parathyroidectomy (PTX) and radio-thyroidectomy (131I-TX) as well as the actions of parathyroid extract (PTE), dibutyryl cyclic adenosine monophosphate (DBcAMP), calcitonin (CT) and thyroid extract (thyreoidea sicca) on effective intestinal calcium absorption in intact, PTX and 131I-TX rats were evaluated by a new, physiological in vivo method. Ten hours after the administration of 47calcium labelled food the animals were killed and the entire intestine was removed. Whole body retention of 47calcium was measured allowing the calculation of the effective intestinal absorption of calcium (true absorption minus excretion within ten hours). The known actions of PTE and DBcAMP were confirmed by this method. CT did not exert a direct effect in any of the experimental groups. The absence of thyroid hormones (TX rats) remarkably reduced effective calcium absorption. In the presence of endogenous parathyroid hormone (PTH) (TX rats) the administration of minimal amounts of thyroid hormones was sufficient to increase effective calcium absorption, whereas PTE and DBcAMP did not have any effect. In the absence of PTH (TX-PTX rats) thyroid hormones did not enhance effective absorption, indicating, that thyroid hormones alone do not stimulate the effective absorption of calcium. It is concluded, that the thyroid hormones act indirectly, as a permissive agent, enabling PTH to exert its active stimulating effect on the effective intestinal absorption of calcium.


1970 ◽  
Vol 48 (4) ◽  
pp. 541-544 ◽  
Author(s):  
M. WINTER ◽  
E. MORAVA ◽  
G. SIMON

SUMMARY The effect of 20 i.u. vitamin D3 on the intestinal absorption of calcium was investigated in thyroidectomized and control rachitic rats. Vitamin D3 increased both duodenal and jejunal calcium absorption in the absence of the thyroid glands. These results suggest that neither thyroxine nor calcitonin are necessary for the effect of vitamin D3 on intestinal calcium absorption.


1984 ◽  
Vol 246 (5) ◽  
pp. R680-R683 ◽  
Author(s):  
F. Bronner

Transmural calcium movement in the intestine involves both saturable and nonsaturable components, with the saturable movement subject to regulation by vitamin D and indirectly by parathyroid hormone. Under conditions of high-calcium intake, calcium absorption due to the saturable component is minimized and the numerical value of the nonsaturable component can equal that found in vitamin D-deficient or parathyroidectomized (PTX) animals on similar calcium intakes. Yet in PTX animals intestinal calcium represents a larger proportion of the calcium inflow into the central pool, and PTX animals are less able to regulate their plasma calcium than hormonally intact animals. This demonstrates that intestinal calcium input in the rat can be classified as a signal disturbing (raising) the plasma calcium.


1958 ◽  
Vol 34 (5) ◽  
pp. 901-909 ◽  
Author(s):  
Ervin Kaplan ◽  
Bernard D. Edidin ◽  
Robert C. Fruin ◽  
Lyle A. Baker

1980 ◽  
Vol 44 (03) ◽  
pp. 146-149 ◽  
Author(s):  
Nicole Ardaillou ◽  
Jeannine Yvart ◽  
Philippe Le Bras ◽  
Marie-José Larrieu

SummaryThe catabolism of human fragment D, (FgD), obtained by plasmin digestion of fibrinogen has been investigated in normal subjects and patients with liver cirrhosis and the results compared with those obtained for fibrinogen (Fg). Fg was labelled with I-125 and Fg D with I-131 using the chloramine T method. The plasma disappearance curves of both labelled proteins fitted a two exponential curve. In controls the plasma clearance rate of Fg D was greater than that of Fg as shown by the marked difference between the half-lives of these two tracers: 8,9 and 83,5 hours for Fg D and Fg respectively. The fractional catabolic rate of Fg D was 3.38 times the plasma pool per day. In nine patients with liver cirrhosis, catabolism of Fg was not modified. In contrast, catabolism of Fg D was significantly reduced with a half life of 13.0 hours and a low fractional catabolic rate. These results suggest the role of the liver in the catabolism of Fg D in man.


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