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The regulation of growth hormone (GH) by thyroid hormones (THs) has been shown to present species variation. We investigated the regulation of GH in the eel, a representative of an ancient group of teleosts. In vivo administration of triiodothyronine (T(3)) or thyroxine (T(4)) significantly reduced pituitary and serum GH levels, as measured by homologous RIA. In order to investigate the ability of THs to regulate GH production directly at the pituitary level, we used a long-term, serum-free primary culture of eel pituitary cells. Both T(3) and T(4) inhibited GH release in a concentration-dependent manner, producing up to 50% inhibition at 10 nM, with an ED(50) of <0.2 nM, within the range of their physiological circulating levels. Other hormones also acting via the nuclear receptor superfamily, such as sex steroids (testosterone, estradiol and progesterone) and corticosteroid (cortisol), had no effect on GH release in vitro, underlining the specificity of the regulatory effect of THs on GH. Measurement of both GH release and cellular content for calculation of GH production in vitro indicated that THs not only inhibited GH release but also GH synthesis. Dot-blot assay of GH messenger RNA (mRNA) using an homologous eel cDNA probe showed a decrease in GH mRNA levels in cells cultured in the presence of T(3), as compared with control cells. This demonstrated that the inhibition of T(3) on GH synthesis was mediated by a decrease in GH mRNA steady state levels. In conclusion, we demonstrate inhibitory regulation of eel GH synthesis and release by THs, exerted directly at the pituitary level. These data contrast with the rat, where THs are known to have a stimulatory effect and suggest that the pattern observed here in an early vertebrate and also found in birds, reptiles and some mammals including humans, may represent an ancestral and more generalized vertebrate pattern of TH regulation of pituitary GH.
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Insulin-like growth factor (IGF)-I has been suggested as a potential signal linking growth and puberty in mammals. Using the juvenile European eel as a model, we employed a long-term, serum-free primary culture of pituitary cells to study the direct effect of IGF-I on gonadotrophin (GtH-II=LH) production. IGF-I increased both cell content and release of GtH-II in a time- and dose-dependent manner. IGF-I and IGF-II had similar potencies but insulin was 100-fold less effective, suggesting the implication of an IGF type 1 receptor. Other growth and metabolic factors, such as basic fibroblast growth factor and thyroid hormones, had no effect on GtH-II production. IGF-I did not significantly increase the number of GtH-II immunoreactive cells, indicating that its stimulatory effect on GtH-II production does not result from gonadotroph proliferation. Comparison of IGF-I and somatostatin (SRIH-14) effects showed that both factors inhibited growth hormone (GH) release but only IGF-I stimulated GtH-II production by eel pituitary cells. This indicates that the effect of IGF-I on gonadotrophs is not mediated by the reduction of GH released by somatotrophs into the culture medium. This study demonstrates a specific stimulatory effect of IGF-I on eel GtH-II production, played out directly at the pituitary level. These data obtained in a primitive teleost suggest that the role of IGF-I as a link between body growth and puberty may have been established early in the evolution of vertebrates.
Medicine, Stopford Building, University of Manchester, Manchester M13 9PT, UK
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Medicine, Stopford Building, University of Manchester, Manchester M13 9PT, UK
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Medicine, Stopford Building, University of Manchester, Manchester M13 9PT, UK
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Medicine, Stopford Building, University of Manchester, Manchester M13 9PT, UK
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Medicine, Stopford Building, University of Manchester, Manchester M13 9PT, UK
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Medicine, Stopford Building, University of Manchester, Manchester M13 9PT, UK
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Medicine, Stopford Building, University of Manchester, Manchester M13 9PT, UK
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Recent studies have suggested that the adipocyte-derived hormone, leptin, plays a role in the regulation of metabolism. Here, we tested this hypothesis in the seasonally breeding Siberian hamster, as this species exhibits profound seasonal changes in adiposity and circulating leptin concentrations driven by the annual photoperiodic cycle. Male hamsters were kept in either long (LD) or short (SD) photoperiods. Following exposure to short photoperiods for 8 weeks animals exhibited a significant weight-loss and a 16-fold reduction of serum leptin concentrations. At Week 9, animals in both photoperiods were infused with leptin or PBS via osmotic mini-pump for 14 days. Chronic leptin infusion mimicked LD-like concentrations in SD-housed animals and caused a further decline in body weight and adipose tissue. In LD-housed animals, leptin infusion resulted in a significant elevation of serum concentrations above natural LD-like levels, but had no discernable effect on body weight or overall adiposity. Both bending and compression characteristics and histomorphometric measurements of trabecular bone mass were unaltered by leptin treatment or photoperiod. Our data therefore show that despite a high natural amplitude cycle of leptin, this hormone has no apparent role in the regulation of bone metabolism, and therefore do not support recent propositions that this hormone is an important component in the metabolism of bone tissue.