Ontogeny of Liver Somatotropic and Lactogenic Binding Sites in Male and Female Rats*

Maes, Marc; Hertogh, R. De; Watrin-Granger, P.; Ketelslegers, J. M.

doi:10.1210/endo-113-4-1325

Cited by 115 publications

(54 citation statements)

References 40 publications

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“…Regulation of rat liver GH receptors by testosterone has not been documented, although it has been reported that females have more receptors than males [1,12,13]. Our studies confirm that testosterone decreases PRL receptors, and they establish a similar role for testosterone on GH binding in the livers of female rats.…”

Section: Discussionsupporting

confidence: 81%

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Adrenal involvement in the diabetes-induced loss of growth hormone and prolactin receptors in the livers of female rats

Bryson

Baxter

1986

Diabetologia

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Summary. Streptozotocin-induced diabetes causes a decrease in growth hormone and prolactin receptors in the livers of female rats, and in the serum concentration of somatomedin-C/ insulin-like growth factor-I, concomitantly with an increase in the serum testosterone levels. In this study, a possible role for adrenal androgens in the loss of receptors was examined. Rats were adrenalectomised bilaterally 3 days after the induction of diabetes with streptozotocin (100mg/kg intravenously), and livers were removed 3 days later. Adrenalectomy had no effect on binding of ovine prolactin or bovine growth hormone to liver microsomal membranes from non-diabetic rats, but in diabetic rats it entirely abolished the 56% decrease in prolactin binding and significantly reversed the 66% decrease in growth hormone binding and the parallel fall in serum levels of somatomedin-C/insulin-like growth factor-I (p<0.05). Adrenalectomy also prevented the diabetes-induced rise in serum testosterone. Daily injection of testosterone to normal and diabetic rats for 12 days significantly reduced both prolactin and growth hormone binding (p< 0.001), with the effect of diabetes being additive upon the testosterone effect. Implantation of testosterone-filled silastic capsules at the time of adrenalectomy (i. e. for 3 days) did not prevent the adrenalectomy-induced restoration of both growth hormone and prolactin receptors. The resulting high serum testosterone level did not reduce binding to growth hormone receptors in control rats over the 3 day period, and caused no further decrease in diabetic rats. However, binding to prolactin receptors was reduced by 47% in control animals with no further loss in diabetic animals (p < 0.001). Adrenalectomy prevented the loss of prolactin receptors in both testosterone-treated and diabetic rats. These results indicate that, whether or not the rise in testosterone of adrenal origin contributes to the receptor loss in diabetes, the effect also depends on another factor of adrenal origin.

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Section: Discussionsupporting

confidence: 81%

“…In contrast to prolactin receptors, little is known about the regulation of G H receptors in rat liver by sex steroids, except that livers from female animals are known to have more receptor sites that those from males when measured in either whole hepatocytes [12] or microsomal membrane preparations [1,13].…”

mentioning

confidence: 99%

Adrenal involvement in the diabetes-induced loss of growth hormone and prolactin receptors in the livers of female rats

Bryson

Baxter

1986

Diabetologia

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“…Newborn infants have undetectable levels of GH-BP [13,15,23], which is consistent with the absence of GH receptors in sheep [24] and rat [25] fetuses. In the developing human [13,15,23] and rat [4,25] both GH-receptors and GH-BP gradually increase, as is the case for the corresponding mRNAs [12].…”

supporting

confidence: 52%

“…In the developing human [13,15,23] and rat [4,25] both GH-receptors and GH-BP gradually increase, as is the case for the corresponding mRNAs [12]. GH-BP is low in patients with anorexia nervosa [26], consistent with the low hepatic GH receptors in undernourished rats [27].…”

mentioning

confidence: 82%

The Clinical Significance of Growth Hormone Binding Protein

Hochberg

Amit

1993

Clin Pediatr Endocrinol

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Abstract. The clinical significance of Growth Hormone Binding Protein (GHBP) is seen in at least three distinct, yet interrelated ways. First, GHBP serves as a serum marker for the GH-receptor level: it is absent in most patients with GH-receptor deficient Laron type dwarfism; it is low in liver cirrhosis, hypothyroidism and malnutrition, where GH-receptor insufficiency has been shown; it is high in hyperthyroidism and obesity, where GH-receptor is increased: and it increases with GH therapy, as reported for rat GH-receptor. Secondly, GHBP slows serum GH clearance and, hence, sustains higher GH levels; serum GHBP correlates negatively with GH disappearance rate, and was suggested as a pharmacological enhancer of GH activity. Finally, GHBP competes with the GH-R on GH binding, and interferes with GH biological activity: in vitro GHBP decreases GH activity, in the rat increasing levels of GHBP result in GH resistance, and in human serum, increasing levels of GHBP diminish GH bioactivity, as measured in vitro by the potency to displace hGH from GH-receptor. We suggest an algorithm to correct RIA-GH levels for the interference effect of GHPB on its biological activity. Our study of normal short children and GHD disclosed negative correlation with serum GH and higher levels in girls then in boys. GHBP did not predict growth response to hGH therapy. It is concluded that the significance of GHBP and its impact on GH bioavailibility and activity is complex, and involves consideration of the GH-receptors, GH volume distribution, GH clearance and competition with the GH-receptors. [51]. The amino acid sequence of the rabbit GH-BP has been shown to be identical with the extracellular domain of the GHreceptor [6].The mechanism of GH-BP synthesis and secretion is not fully understood.

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“…The increase of GHR mRNA in liver also paralleled the postnatal increase in G H binding sites on female liver membranes (17), suggesting a close relationship between GHR mRNA abundance and receptor protein concentrations. Similarly, the comparatively low GHR mRNA abundance observed in the other tissues is consistent with the low levels of G H binding reported for nonhepatic tissues (7).…”

Section: Methodsmentioning

confidence: 74%

Tissue-Specific Developmental Regulation of the Messenger Ribonucleic Acids Encoding the Growth Hormone Receptor and the Growth Hormone Binding Protein in Rat Fetal and Postnatal Tissues

et al. 1992

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ABSTRACT. Tissue responsiveness to growth hormone is likely to be regulated by local concentrations and availability of the membrane-bound growth hormone receptor (GHR) and perhaps by the actions of the soluble growth hormone binding protein (GHBP). To determine whether the developmental regulation of the GHR and GHBP might vary among tissues, we have measured the relative abundance of the 4.3-kb GHR and 1.3-kb GHBP mRNA in rat fetal and postnatal liver, kidney, lung, and ileum by Northern hybridization of polyadenylated RNA with a 32P-labeled antisense riboprobe prepared from a rat GHR cDNA. The GHR and GHBP mRNA were both present in the four tissues studied at fetal age 19 d (E19). In postnatal liver, both transcripts increased in abundance 3-to 4-fold after 14 d to mature levels at 42 d ( p = 0.0001). Similar changes were seen in postnatal kidney for GHR mRNA abundance; however, GHBP mRNA abundance increased only 2-to 3-fold to mature levels by 28 d (kidney GHR versus GHBP mRNA profile, p = 0.0001). In lung, a 2-fold linear increase in GHR mRNA abundance was observed (p = 0.0019), but the GHBP mRNA did not change (GHR versus GHBP mRNA profile, p = 0.0006). Both transcripts decreased in abundance by 2-to 3-fold from E l 9 to 42 d in ileum (p < 0.05). The abundance of both transcripts was three to 10 times greater in 60-d liver than in the other three tissues at 60 d. The variation in abundance and in the developmental profiles of the GHR and GHBP mRNA observed in these fetal and postnatal tissues suggests that the GHR and GHBP could mediate differences within and between tissues in the responsiveness to growth hormone. The differential regulation of the two transcripts evident in kidney and lung supports the emerging evidence that the GHBP may have a function distinct from that of the GHR. (Pediatr Res 31: 335-339, 1992) Abbreviations GH, growth hormone GHR, growth hormone receptor GHBP, growth hormone binding protein poly A+, polyadenylated RNA

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Ontogeny of Liver Somatotropic and Lactogenic Binding Sites in Male and Female Rats*

Cited by 115 publications

References 40 publications

Adrenal involvement in the diabetes-induced loss of growth hormone and prolactin receptors in the livers of female rats

Adrenal involvement in the diabetes-induced loss of growth hormone and prolactin receptors in the livers of female rats

The Clinical Significance of Growth Hormone Binding Protein

Tissue-Specific Developmental Regulation of the Messenger Ribonucleic Acids Encoding the Growth Hormone Receptor and the Growth Hormone Binding Protein in Rat Fetal and Postnatal Tissues

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