PERINATAL ONTOGENY OF PORCINE GROWTH-HORMONE RECEPTOR GENE-EXPRESSIONIS MODULATED BY THYROID STATUS

Citation
C. Duchamp et al., PERINATAL ONTOGENY OF PORCINE GROWTH-HORMONE RECEPTOR GENE-EXPRESSIONIS MODULATED BY THYROID STATUS, European journal of endocrinology, 134(4), 1996, pp. 524-531
Citations number
39
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
08044643
Volume
134
Issue
4
Year of publication
1996
Pages
524 - 531
Database
ISI
SICI code
0804-4643(1996)134:4<524:POOPGR>2.0.ZU;2-J
Abstract
The ontogeny of growth hormone receptors (GHR) represents a critical s tage in growth and metabolism. We have investigated the perinatal onto geny of hepatic and skeletal muscle GHR gene expression in piglets, an d its modulation by GH and thyroid hormones. Test piglets were rendere d hypothyroid in late gestation by feeding the sow a high-glucosinolat e rapeseed meal, Plasma and tissue samples were obtained from test and control piglets at various ages between 80 days of fetal life (80F) a nd 2 days postnatally. Plasma hormone levels were determined by radioi mmunoassay and GHR mRNA by RNase protection assays, In controls, plasm a thyroxine (T-4) and 3,5,3'-triiodothyronine (T-3) levels increased b etween 80F and birth and the early postnatal period was characterized by a marked surge in plasma T-3. Test piglets were hypothyroid at 110F with total T-4, total T-3 and free T-3 levels being reduced by 28, 53 and 33% respectively. By contrast, the postnatal increase in T-3 was more marked in test than in control animals, Plasma GH levels decrease d over the perinatal period and there was no effect of treatment, Hepa tic GHR mRNA was at the lower limit of detection at 80F but by 110F wa s expressed in both groups of animals, However, fetal hypothyroidism a t 110F resulted in a marked 70% decrease in hepatic GHR mRNA (p < 0.01 ), The higher postnatal rise in T-3 in test piglets was accompanied by a recovery of hepatic GHR mRNA levels. By contrast with liner, skelet al muscle (longissimus dorsi) expressed high levels of GHR mRNA at 80F and hypothyroidism induced a 68% increase in GHR mRNA (p < 0.001), Th e present results suggest that thyroid hormones may modulate the perin atal ontogeny of GHR gene expression, in addition to other hormonal fa ctors, and that this modulation is tissue-specific.