Effect of bovine somatotropin (bST) on autocrine/paracrine secretion of insulin-like growth factor-I (IGF-I) by the mammary gland of dairy cows

1993 ◽  
Vol 35 (1-2) ◽  
pp. 178-179
1990 ◽  
Vol 126 (3) ◽  
pp. 437-443 ◽  
Author(s):  
C. G. Prosser ◽  
I. R. Fleet ◽  
A. N. Corps ◽  
E. R. Froesch ◽  
R. B. Heap

ABSTRACT The close-arterial infusion of free insulin-like growth factor-I (IGF-I; 1·1 nmol/min) for 6 h into the pudic artery supplying one mammary gland of lactating goats caused a 25±6% (mean ± s.e.m., n = 6) increase in the rate of milk secretion of that gland. The increase in the rate of milk secretion in the adjacent non-infused gland (14±4%) was not significantly different from that observed during saline infusion (4±5%). Blood flow to the infused gland was increased from 378±26 ml/min 1 h before to 487±56 ml/min approximately 5 h after the start of the infusion of IGF-I, declining to 420±44 ml/min approximately 2 h after the end of the infusion. The total concentration of IGF-I (free and bound) in milk of the infused gland was significantly higher than that of the non-infused gland. The concentrations of IGF-I in carotid arterial plasma samples increased during IGF-I infusion from a mean value of 32±2 nmol/l before to a maximum of 49±3 nmol/l 5 h after the infusion commenced. Circulating concentrations of total IGF-I declined slowly after the infusion with an estimated half-life of 5 h. Infusion of saline alone did not alter mammary blood flow or the concentration of total IGF-I in milk or plasma. The results indicate that the infusion of free IGF-I into the mammary arterial supply enhances milk secretion and mammary blood flow in intact, conscious goats. The more pronounced effect in the infused compared with the non-infused gland suggests that free IGF-I acts directly on the mammary gland. The response in the non-infused gland was attenuated presumably due to association of IGF-I with plasma binding proteins during recirculation. Journal of Endocrinology (1990) 126, 437–443


2003 ◽  
Vol 15 (9) ◽  
pp. 21
Author(s):  
F. Y. Obese ◽  
T. E. Moyes ◽  
C. S. Pino ◽  
C. R. Stockdale ◽  
K. L. Macmillan ◽  
...  

2015 ◽  
Vol 98 (8) ◽  
pp. 5422-5428 ◽  
Author(s):  
R. Murney ◽  
K. Stelwagen ◽  
T.T. Wheeler ◽  
J.K. Margerison ◽  
K. Singh

Endocrinology ◽  
2001 ◽  
Vol 142 (4) ◽  
pp. 1479-1488 ◽  
Author(s):  
Darryl L. Hadsell ◽  
Tatiana Alexeenko ◽  
Yann Klemintidis ◽  
Daniel Torres ◽  
Adrian V. Lee

Abstract Overexpression of des(1–3) human insulin-like growth factor I (IGF-I) in the mammary glands of transgenic mice (WAP-DES) inhibits apoptosis during natural, but not forced, mammary involution. We hypothesized that this differential response would correlate with the expression of IGF signal transducers. Forced and natural involution were analyzed in nontransgenic and WAP-DES mice beginning on day 16 postpartum. During natural involution, mammary gland wet weight was higher and apoptosis was lower in WAP-DES than in nontransgenic mice. The WAP-DES transgene had no effect on these parameters during forced involution. Mammary tissue concentrations of the transgene protein were 2- to 10-fold higher than those of endogenous IGF-I. Western blot analysis of pooled mammary tissue extracts demonstrated only slightly higher phosphorylation of the IGF signal transducers insulin receptor substrate-1 (IRS-1) and Akt in the WAP-DES than in nontransgenic mice. Dramatic early reductions in phospho-IRS-1, phospho-Akt, IRS-1, IRS-2, and Akt proteins occurred during forced, but not natural, involution. The abundance of the IGF-I receptor and the messenger RNAs for the IGF-I receptors, IRS-1 and -2, were not affected by either genotype or involution. These findings support the conclusions that mammary cells lose their responsiveness to insulin-like signals during forced involution, and that posttranscriptional or posttranslational regulation of IRS-1 and IRS-2 may play a role in this loss.


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