scholarly journals Plasma Growth Hormone and Insulin-Like Growth Factor-I Responses to Bovine Growth Hormone-Releasing Factor and Its Analogs in Dairy Cattle

1992 ◽  
Vol 63 (6) ◽  
pp. 576-584
Author(s):  
Koichi HODATE ◽  
Tetsu JOHKE ◽  
Akihito OZAWA ◽  
Hiroshi FUSE ◽  
Yoshiaki OBARA ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Dairy Cattle ◽  
Bovine Growth Hormone ◽  
Insulin Like Growth Factor ◽  
Plasma Growth Hormone ◽  
Growth Hormone Releasing Factor ◽  
Factor I ◽  
Growth Factor I

Growth Hormone-Releasing Factor Regulation by Somatostatin, Growth Hormone and Insulin-Like Growth Factor I in Fetal Rat Hypothalamic-Brain Stem Cell Cocultures

1993 ◽  
Vol 58 (6) ◽  
pp. 655-665 ◽  
Author(s):  
Gumersindo Fernández Vázquez ◽  
Luanda Cacicedo ◽  
Maria Teresa de los Frailes ◽  
Maira Jesús Lorenzo ◽  
Rosa Tolón ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Stem Cell ◽  
Growth Factor ◽  
Brain Stem ◽  
Insulin Like Growth Factor ◽  
Growth Hormone Releasing Factor ◽  
Factor I ◽  
Fetal Rat ◽  
Growth Factor I

Increased secretion of insulin-like growth factor I into milk of cows treated with recombinantly derived bovine growth hormone

1989 ◽  
Vol 56 (1) ◽  
pp. 17-26 ◽  
Author(s):  
Colin G. Prosser ◽  
Ivan R. Fleet ◽  
Anthony N. Corps
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Milk Yield ◽  
Plasma Concentrations ◽  
Significant Proportion ◽  
Bovine Growth Hormone ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

SummarySix lactating, non-pregnant Jersey cows were given subcutaneous injections of recombinantly derived bovine growth hormone for 7 d. Milk yield was increased by 4·5 kg/d on d 7, compared with the average yield of 10·7 ± 0·4 kg/d (mean ± s. e. m.) for the 7d preceding treatment. Concentrations of insulin-like growth factor I (IGF-I) in the milk increased from 0·44 ± 0·04 nmol/1 (mean ± s. e. m.) during the 7 d preceding treatment to 1·6 ± 0·2 nmol/1 on d 7 of treatment. Taking the increase in milk yield into account the total increase in the secretion of IGF-I into milk of one udder half was 6-fold. Plasma concentrations of total IGF-I rose from 15·5 + 1·3 nmol/1 (mean ± s. e. m.) on the day preceding treatment to 56·9 ± 3·6 nmol/1 (mean ± s. e. m.) on d 7 of treatment. Mammary plasma flow increased from 1·6 ± 0·09 to 2·2 ± 0·06 1/min udder half over the same time. Estimates of the amount of IGF-I that reached the mammary gland gave values of 24 and 116 nmol/min udder half before and during treatment respectively. IGF-I in milk of treated cows was associated predominantly with proteins ranging from 40000 to 150000 mol. wt, but a significant proportion (19%) of the total IGF-I was present in the free unbound form. IGF-I crosslinking studies revealed the presence in milk of one specifically labelled band at 31000 mol. wt.

Characteristics of phorbol ester stimulated growth hormone release: inhibition by insulin-like growth factor I, somatostatin, and low calcium medium and comparison with growth hormone releasing factor

1987 ◽  
Vol 65 (11) ◽  
pp. 2302-2307 ◽  
Author(s):  
M. S. Sheppard ◽  
B. A. Eatock ◽  
R. M. Bala
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Inositol Phosphate ◽  
Cell System ◽  
Channel Blockers ◽  
Insulin Like Growth Factor ◽  
Growth Hormone Releasing Factor ◽  
Factor I ◽  
Low Calcium ◽  
Growth Factor I

TPA (12-O-tetradecanoylphorbol 13-acetate) is one of a class of compounds known as tumor promoters which perturb the inositol phosphate pathway in a number of cells. We have used TPA in a dispersed rat adenohypophysial cell system to probe the characteristics of growth hormone (GH) release. In this system we have found that the cells release GH in response to low concentrations of TPA: the EC50 was 0.23 ± 0.05 nM (n = 6) and the maximal concentration was 5 nM. However, the maximal TPA-induced GH release was only 34 ± 5% (n = 7) of the GH released by maximal growth hormone releasing factor (GRF) suggesting TPA releases a subpool of stored GH. Both somatostatin and insulin-like growth factor I inhibit GH release stimulated by TPA to the same extent as that stimulated by GRF, showing that the normal inhibitory control mechanism of release is not altered. Incubation in a low calcium medium that totally blocks GRF-stimuiated GH release also inhibits TPA-stimulated GH release. The calcium channel blockers nifedipine and diltiazem both partly inhibit GRF- and TPA-stimulated GH release, showing some component of the calcium necessary for GH release arises from influx across the cell membrane.

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