The relationship of growth hormone to 1,25-dihydroxyvitamin D3 in intestinal calcium transport

1981 ◽  
Vol 3 (1) ◽  
pp. 47-49 ◽  
Author(s):  
J.K. Yeh ◽  
J.F. Aloia
2013 ◽  
Vol 31 (8) ◽  
pp. 685-691 ◽  
Author(s):  
Narattaphol Charoenphandhu ◽  
Kamonshanok Kraidith ◽  
Jarinthorn Teerapornpuntakit ◽  
Kanogwun Thongchote ◽  
Pissared Khuituan ◽  
...  

1959 ◽  
Vol 196 (2) ◽  
pp. 231-234 ◽  
Author(s):  
N. Altszuler ◽  
R. Steele ◽  
A. Dunn ◽  
J. S. Wall ◽  
R. C. de Bodo

The mechanism whereby growth hormone diminishes the hypoglycemic effect of insulin was investigated in hypophysectomized dogs using a C14 glucose dilution technique. An intravenous injection of insulin into the normal dog increased the rate of glucose utilization, and the resulting hypoglycemia was promptly abolished by an increased rate of glucose production. In the hypophysectomized dog prior to growth hormone administration, the insulin injection increased the rate of glucose utilization to a greater extent than in the normal animal, while the ability to increase the rate of glucose production was shown to be limited. In the hypophysectomized dog, a growth hormone regimen (1 mg/kg/day for 4 days) increased the rate of glucose production and utilization. The intravenous injection of insulin during the growth hormone regimen resulted in a lesser increase in the rate of plasma glucose utilization than observed prior to the growth hormone regimen. Furthermore, the growth hormone regimen improved the animal's limited ability to increase glucose production in response to the insulin-induced hypoglycemia. These effects of growth hormone contribute to the decreased effectiveness of insulin. The relationship of the ‘anti-insulin’ effect of growth hormone to its influence on glucose turnover is discussed.


1983 ◽  
Vol 244 (2) ◽  
pp. E159-E163
Author(s):  
S. Okamoto ◽  
Y. Tanaka ◽  
H. F. DeLuca ◽  
Y. Kobayashi ◽  
N. Ikekawa

The biological activity of 24,24-difluoro-1,25-dihydroxyvitamin D3 was compared with 1,25-dihydroxyvitamin D3 in the rat. The 24,24-difluoro-1,25-dihydroxyvitamin D3 has a potency of approximately 5-10 times that of 1,25-dihydroxyvitamin D3 in the known in vivo vitamin D responsive systems. These systems include intestinal calcium transport, bone calcium mobilization, calcification of epiphyseal plate cartilage, and elevation of plasma calcium and phosphorus concentrations. Thus, 24,24-difluoro-1,25-dihydroxyvitamin D3 is the first known analogue with higher potency than 1,25-dihydroxyvitamin D3 in vivo.


1988 ◽  
Vol 254 (4) ◽  
pp. E402-E406
Author(s):  
H. F. DeLuca ◽  
R. R. Sicinski ◽  
Y. Tanaka ◽  
P. H. Stern ◽  
C. M. Smith

The biological activity of 1,25-dihydroxyvitamin D2 [1,25(OH)2D2] and 24-epi-1,25-dihydroxyvitamin D2 [24-epi-1,25(OH)2D2] has been determined in vitamin D-deficient rats. The biological effectiveness of 1,25(OH)2D2 is equal to that reported previously for 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] (15) in intestinal calcium transport, mineralization of bone, mobilization of bone calcium, and elevation of plasma inorganic phosphorus of rachitic rats. However, 24-epi-1,25(OH)2D2 is at best one-half as active as 1,25(OH)2D2 in stimulating intestinal calcium transport and in the mineralization of rachitic bone. The 24-epi-1,25(OH)2D2 is one-third as active as 1,25(OH)2D3 in binding to the chick intestinal receptor for 1,25(OH)2D3. Thus receptor discrimination may account for the twofold difference in intestinal calcium transport activity. 24-Epi-1,25(OH)2D2 appeared inactive in in vivo mobilization of bone calcium or bone phosphorus. On the other hand, in fetal rat bone in culture, the epi compound was only five times less active than 1,25(OH)2D2 in inducing resorption. Short-term experiments on bone mineral mobilization in vivo show that the 24-epi-1,25(OH)2D2 does induce bone calcium mobilization but that its activity in this respect is short lived. It is suggested that 24-epi-1,25(OH)2D2 and, as a result, it shows preferential activity on intestine whose response to a single dose of 1,25(OH)2D2 remains for several days, whereas the short-lived bone system does not remain stimulated during the 24-h period between doses.


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