Genetic variation in stimulated GH release and in IGF-I of young dairy cattle and their associations with the leucine/valine polymorphism in the GH gene.

2001 ◽  
Vol 79 (2) ◽  
pp. 470 ◽  
Author(s):  
R Grochowska ◽  
P Sørensen ◽  
L Zwierzchowski ◽  
M Snochowski ◽  
P Løvendahl
Keyword(s):  
Igf I ◽  
1990 ◽  
Vol 122 (6) ◽  
pp. 745-752 ◽  
Author(s):  
Patrick Pagesy ◽  
Jacques Y. Li ◽  
Françoise Rentier-Delrue ◽  
Olivier Delalande ◽  
Yves Le Bouc ◽  
...  

Abstract. Some patients with active acromegaly have elevated plasma IGF-I concentrations with only minimal elevation of plasma GH. We compared adenomatous GH and SRIH expression in 3 such patients (patients No. 1, 2 and 3; basal plasma GH level < 4 μg/l) and in 3 acromegalic patients with high basal plasma GH level (patients No. 4, 5 and 6; 51.7 ± 16.1 μg/l, mean ± sem). By immunocytochemistry, all the tumours proved to be somatotropic adenomas. At the ultrastructural level, signs of low secretory activity were observed in adenomas from patients No. 2 and 3. Perifused adenoma cells of patients No. 1, 2 and 3 released very little GH compared with those of patients No. 4, 5 and 6 (1± 0.37 vs 51.5± 34.1 μg · (10−6 cells) · min−1, p< 0.001). Adenoma SRIH content was 65.7 and 30.6 pg/mg proteins in patients No. 1 and 2, whereas it was undetectable in the others (patients No. 4, 5 and 6). Northern blot analysis showed that the GH gene was poorly expressed in the adenomas from patients No. 1, 2 and 3 compared with the adenomas from patients No. 4, 5 and 6. SRIH mRNA was detected in all 6 adenomas. However, the signal was more intense in the adenomas from patients No. 1, 2 and 3 than in those from patients No. 4, 5 and 6. In conclusion, because of the variability of the biosynthetic and secretory potential of the somatotropic adenomas, patients harbouring this type of pituitary tumours can exhibit a wide range of plasma GH levels. In acromegaly with minimal elevation of plasma GH, the synthesis of SRIH by the adenoma cells themselves could play a role in the inhibition of GH expression.


1997 ◽  
Vol 153 (2) ◽  
pp. 251-257 ◽  
Author(s):  
Y Hong ◽  
K Brismar ◽  
K Hall ◽  
N L Pedersen ◽  
U de Faire

Abstract It has previously been shown that the serum levels of insulin-like growth factor-I (IGF-I), IGF-binding protein-1 (IGFBP-1), and insulin are influenced by genetic effects to various degrees. From a clinical and preventive point of view, however, it is important to identify potentially modifiable non-genetic factors influencing the levels of these measures. Because monozygotic twin pairs share the same genetic background, differences in phenotypic levels within monozygotic twin pairs are believed to be due to non-genetic influences. Accordingly, the associations between intrapair differences in one phenotype and intrapair differences in another phenotype are also due to non-genetic influences. The present sample of 97 pairs of monozygotic twins from the population-based Swedish Adoption/Twin Study of Aging (SATSA) provided the opportunity to assess non-genetic influences on the levels of IGF-I, IGFBP-1, and insulin. Several metabolic measures were found to account for the variation of IGF-I, IGFBP-1, and insulin after controlling for the genetic influences. IGFBP-1 and glucose were significant predictors for the levels of IGF-I. IGFBP-1 and glucose together explained about one quarter of the non-genetic variation of IGF-I. However, when IGFBP-1 was dropped from the regression model, insulin was the only independent predictor of IGF-I, and explained about 19% of the non-genetic variation for IGF-I. For IGFBP-1, insulin and IGF-I were the significant non-genetic predictors. Insulin and IGF-I explained about 28 and 8% respectively of the non-genetic variation for IGFBP-1, while for insulin, IGF-I, triglycerides, body height, glucose, and body mass index (BMI) explained approximately 20, 12, 6, 5 and 5% respectively of the non-genetic variation. Journal of Endocrinology (1997) 153, 251–257


2003 ◽  
Vol 52 (6) ◽  
pp. 489-500 ◽  
Author(s):  
Yves Barrière ◽  
Jean-Claude Emile ◽  
Fabien Surault

Endocrinology ◽  
2007 ◽  
Vol 149 (3) ◽  
pp. 1366-1376 ◽  
Author(s):  
Zhuohua Wang ◽  
Raul M. Luque ◽  
Rhonda D. Kineman ◽  
Vera H. Ray ◽  
Konstantin T. Christov ◽  
...  

We asked whether down-regulation of GH signaling could block carcinogenesis in the Probasin/TAg rat, a model of aggressive prostate cancer. The Spontaneous Dwarf rat, which lacks GH due to a mutation (dr) in its GH gene, was crossed with the Probasin/TAg rat, which develops prostate carcinomas at 100% incidence by 15 wk of age. Progeny were heterozygous for the TAg oncogene and homozygous for either the wild-type GH gene (TAg/Gh+/+) or the dr mutation (TAg/Ghdr/dr). Prostate tumor incidence and burden were significantly reduced, and tumor latency was delayed in TAg/Ghdr/dr rats relative to TAg/Gh+/+ controls. At 25 wk of age, loss of GH resulted in a 20 and 80% decrease in the area of microinvasive carcinoma in the dorsal and lateral lobes, respectively. By 52 wk of age, invasive prostate adenocarcinomas were observed in all TAg/Gh+/+ rats, whereas the majority of TAg/Ghdr/dr did not develop invasive tumors. Suppression of carcinogenesis could not be attributed to alterations in prostate expression of TAg or androgen receptor or changes in serum testosterone levels. As carcinogenesis progressed in TAg/Gh+/+ rats, prostate GHR mRNA and protein expression increased significantly, but prostate IGF-I receptor mRNA and protein levels dropped. Furthermore, serum IGF-I and prostate IGF-I levels did not change significantly over the course of carcinogenesis. These findings suggest that GH plays a dominant role in progression from latent to malignant prostate cancer driven by the powerful probasin/TAg fusion gene in rats and suggest that GH antagonists may be effective at treating human prostate cancer.


1997 ◽  
Vol 41 (2) ◽  
pp. 301-301
Author(s):  
S B Oliveira ◽  
I J P Arnhold ◽  
J A Phillips ◽  
B B Mendonça

1977 ◽  
Vol 28 (6) ◽  
pp. 1107 ◽  
Author(s):  
ND Herron ◽  
WA Pattie

The structure of the pedigree Australian Illawarra Shorthorn breed in Australia was analysed by using registration data from the Society's Herd Books. The breed may be divided into three broad levels, namely, Breeders' Herds, Multipliers' Herds and Grade (unregistered) Herds. Of the registered herds, 32% are Breeders' Herds and the remainder are Multipliers' Herds. These are each subdivided into four strata depending on their importance as a source of breeding material, and on their registration practices respectively. Of major importance is the highest stratum of the breed. It comprised only 13.6% of all herds, but accounted for 40.5% of male and 24.8% of female registrations. There is a high ratio of females to males registered of 5.9, which indicates considerable selective registration of males. The degree of this selective registration generally increases at the lower strata, ranging from 3.6 at the top of the structure to 8.7 toward the bottom of the structure. Of all new herds initiated from 1931 to 1971, 44% survived less than 5 years. These short-lived herds averaged only 3.3 female registrations per year, but herd size increased as longevity increased. These points highlight the instability of new, small studs, and indicate that few herds are big enough, or exist for long enough, to contribute significantly to breed improvement. It is not likely that there is much genetic variation between herds. Bulls from major breeders' herds are used widely throughout the breed, while 68% of sires and 24% of dams are bred in herds other than the one in which they were used.


1998 ◽  
Vol 43 (2) ◽  
pp. 301-301
Author(s):  
S B Oliveira ◽  
J P Arnhold ◽  
J A Phillips ◽  
B B Mendonca

Sign in / Sign up

Export Citation Format

Share Document