scholarly journals MODULATION OF INSULIN-LIKE GROWTH FACTOR-I (IGF-I) mRNA EXPRESSION FOLLOWING ACUTE HEMIDIAPHRAGM DENERVATION 26

1996 ◽  
Vol 28 (Supplement) ◽  
pp. 5
Author(s):  
L. E. Gosselin ◽  
K. C. Westerlind
1995 ◽  
Vol 146 (2) ◽  
pp. 239-245 ◽  
Author(s):  
J M Brameld ◽  
P A Weller ◽  
J C Saunders ◽  
P J Buttery ◽  
R S Gilmour

Abstract The effects of various hormones commonly added to hepatocyte culture media upon the expression of the GH receptor (GHR) and insulin-like growth factor-I (IGF-I) genes in cultured porcine hepatocytes were investigated. Preliminary investigations indicated that there was an absolute requirement only for insulin, with high losses of cell viability upon long term exclusion of insulin from the culture medium. The decline in GHR expression with time in culture was found to be less when high levels of glucose were included in the medium. Therefore the basal culture medium used in these studies was Williams' medium E supplemented with 0·2% (w/v) BSA, 5000 mg glucose/l and 100 nmol porcine insulin/l. The addition of dexamethasone (100 nmol/l) increased the expression of both GHR and IGF-I (class 1 transcripts only) mRNA (P<0·001 and P<0·05 respectively), and resulted in an increased responsiveness of IGF-I mRNA expression to GH (1 μg/ml), when the two were added in combination (although only class 1 transcripts were shown to be statistically significant, P<0·01). The addition of either thyroid hormone (1 nmol/l T3 or T4) alone also increased the expression of GHR mRNA (P<0·01) in addition to the dexamethasone stimulated expression, with T4 appearing to decrease IGF-I expression slightly (P<0·05) (either on its own or with T3). As with dexamethasone, the thyroid hormones increased the response of IGF-I mRNA expression to GH (1 μg/ml) when added in combination with GH (P<0·001). These observations demonstrate one possible mechanism for the interactions of glucocorticoids and thyroid hormones with the GH–IGF axis. Journal of Endocrinology (1995) 146, 239–245


1995 ◽  
Vol 132 (5) ◽  
pp. 605-610 ◽  
Author(s):  
Lorenz C Hofbauer ◽  
Michael Rafferzeder ◽  
Onno E Janssen ◽  
Roland Gärtner

Hofbauer LC, Rafferzeder M, Janssen OE, Gartner R. Insulin-like growth factor I messenger ribonucleic acid expression in porcine thyroid follicles is regulated by thyrotropin and iodine. Eur J Endocrinol 1995;132:605–10. ISSN 0809–4643 Insulin-like growth factor I (IGF-I) has been shown to be released from thyrocytes in vitro. We investigated IGF-I mRNA expression during treatment with thyrotropin (TSH), forskolin and potassium iodide (KI) in intact porcine thyroid follicles ex vivo. Porcine thyroid follicles were prepared by collagenase digestion and cultured in the presence of TSH, forskolin or KI. After different incubation times, mRNA was isolated and examined by Northern hybridization with a porcine IGF-I cDNA probe of 405 bp in length. In untreated follicles no IGF-I mRNA was found, whereas in follicles stimulated with TSH an IGF-I mRNA of 7.0 kb was detected after 24 h, which persisted for another 24 h. Forskolin treatment mimicked the TSH effect, indicating that IGF-I mRNA expression may be stimulated by the adenylate cyclase pathway. Preincubation of the porcine follicles with KI decreased dose dependently the TSH-induced IGF-I mRNA expression, with complete inhibition at 10 μmol/l KI. These results suggest that TSH acts via the cAMP pathway to enhance IGF-I mRNA expression, which then may lead to an autocrine IGF-I stimulation. The IGF-I mRNA expression is under negative control of iodide. Roland Gärtner, Medizinische Klinik, Ludwig Maximilians University, Ziemssenstrasse 1, 80336 München, Germany


Bone ◽  
1994 ◽  
Vol 15 (6) ◽  
pp. 647-653 ◽  
Author(s):  
H. Tanaka ◽  
R. Quarto ◽  
S. Williams ◽  
J. Barnes ◽  
C.T. Liang

1993 ◽  
Vol 139 (2) ◽  
pp. 243-252 ◽  
Author(s):  
C. Duan ◽  
E. M. Plisetskaya

ABSTRACT In salmonids, nutritional insufficiency leads to retarded growth and reduced hepatic GH receptors, but increased circulating GH levels. To understand the endocrine mechanism underlying the retarded growth in starved fish better, we investigated the effect of food deprivation and refeeding on circulating levels of GH and insulin, as well as insulin-like growth factor-I (IGF-I) mRNA expression in different tissues of juvenile coho salmon (Oncorhynchus kisutch). Deprivation of food for 2–4 weeks resulted in cessation of growth and a significant decrease in condition factor (an indicator of fish body shape). No difference in circulating insulin or glucose levels were found between starved and fed fish, whereas starvation increased the plasma GH levels. After 4 weeks of starvation, the plasma GH level rose to 9 ng/ml, which was four times as high as that of the fed fish. In spite of elevated circulating GH, hepatic IGF-I mRNA levels were significantly reduced after 4 weeks of starvation. No significant difference in IGF-I mRNA levels of fed and starved fish was found in other tissues, including kidney, spleen, ovary, gill filament and gut. Two weeks of refeeding significantly increased hepatic IGF-I mRNA levels and growth and reduced plasma GH levels. These results suggest that food deprivation primarily reduces IGF-I mRNA expression in the liver which results, most probably, in a decline in systemic IGF-I levels and consequently leads to the retarded growth of salmon. Journal of Endocrinology (1993) 139, 243–252


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