The effect of fasting on liver receptors for prolactin and growth hormone

Baxter, Robert C.; Bryson, Janet M.; Turtle, John R.

doi:10.1016/0026-0495(81)90052-4

Cited by 91 publications

(37 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The insulin levels were decreased in U rats in the postab sorptive state as well as after a 16-hour fast by comparison with D R orC rats, similarly to previous reports [4,13,15], but in contrast to others [16,17], It has been reported that hypoinsulinemia of fast causes a loss of high-affinity GH receptors in the liver and could thereby result in a relative hepatic resistance to GH and a decreased hepatic genera tion of somatomedins [18]. The hypoinsulinemia of U rats in our study could also be associated with a decrease in somatomedin and hence in growth.…”

Section: Discussionsupporting

confidence: 67%

Plasma and Pituitary Content of Growth Hormone Luteinizing Hormone, and Prolactin in Uremic Rats

Lacour

Roullet²,

Bluet-Pajot

et al. 1986

Nephron

View full text Add to dashboard Cite

The influence of chronic renal failure on pituitary content and on serum concentrations of growth hormone (GH), prolactin (PRL), and luteinizing hormone (LH) was studied in chronically uremic rats by comparison with control rats fed ad libitum and diet-restricted rats pair-fed with uremic rats. A decrease of pituitary GH content was found in uremic and diet-restricted rats, in association with a normal circulating GH level. A decrease of pituitary PRL and LH content with respectively high and normal serum values was observed in uremic but not in diet-restricted rats. These data strongly suggest that GH disturbances are related to malnutrition, whereas PRL and LH abnormalities are related to the uremic state per se. As hypoinsulinemia was observed in uremic rats, and as insulin is largely implicated in growth, we have investigated the effects of chronic infusion of insulin, using miniosmotic pumps, on pituitary hormone content. In spite of a normalization of circulating insulin levels in uremic rats treated with insulin, pituitary GH, LH, and PRL contents were unaffected. Thus, insulin deficiency did not appear to be responsible for the diminished pituitary reserve of these hormones.

show abstract

Section: Discussionsupporting

confidence: 67%

Plasma and Pituitary Content of Growth Hormone Luteinizing Hormone, and Prolactin in Uremic Rats

Lacour

Roullet²,

Bluet-Pajot

et al. 1986

Nephron

View full text Add to dashboard Cite

show abstract

“…IGF-binding proteins were partially responsible for the inhibition, but small molecules, characterized by Du Caju, were later shown to be involved as well [201]. Subsequently it was shown by Baxter et al [202]and Maes et al [203]that GH responsiveness was instrumental in the lowering of SM activity, and that there was a decreased SM/IGF responsiveness, suggesting a chain of adaptations of the GH/SM axis resulting in a net decrease of SM action [204]. Extensive studies by the groups of Phillips, Shapiro and Pimstone, Hintz, Takano, Rappaport, Price and their respective co-workers, and many others have contributed to the understanding of the role of SM in nutritional disorders [205, 206, 207, 208, 209, 210].…”

Section: Sf As Endocrine Substancementioning

confidence: 99%

A Personal View on the Early History of the Insulin-Like Growth Factors

Brande¹

1999

Horm Res Paediatr

View full text Add to dashboard Cite

Salmon and Daughaday, when trying to set up an in vitro assay for Growth Hormone (GH), failed to obtain a direct effect on sulphate uptake in cartilage of hypophysectomized (hypox) rats. They recognised that this was not the consequence of poor methodology or materials, but an encrypted message from the examined system. They decided to turn around and to try and decipher it. Treatment with GH appeared to render hypox rat serum active in stimulating sulphation in hypox rat cartilage. They proposed that GH induced an intermediary substance, responsible for this biological effect: sulphation factor (SF), later renamed to Somatomedin(s) (SM). This hypothesis met with great criticism and very few took on to study this hypothetical substance. Besides disbelief, slow progress was also due to initial lack of a practical assay and to the failure to find a tissue with enriched concentration from which to extract the activity. From experimental evidence, the concept gradually evolved that SF/SM was insulin-like and might be identical to NSILA (non-suppressible insulin-like activity). This again generated controversy. This characteristic was too far away from the known effects of GH to be readily acceptable as a physiological phenomenon. The subsequent recognition of the distinct characteristics of the receptors for SM/NSILA and insulin, the discovery of the SM/NSILA binding proteins and, much later, a beginning understanding of their interactions, modifications and breakdown, have gradually resolved this apparent contradiction. When the sequence of two NSILA molecules became known, they were named IGF-I and -II. Structural similarity with proinsulin and identity of IGF-I with SM-C and -A were established and it was found that Multiplication Stimulating Activity (MSA), a growth factor isolated from fetal calf serum and subsequently from conditioned media of a rat liver cell line, was the rat equivalent of IGF-II. Structure-function relations could be studied, a quest which is not yet brought to an end. Meanwhile, the endocrine profile of SF/SM had gradually emerged by measuring plasma levels with bioassays. The main determinants were found to be age, body size, GH and the nutritional state. Later, radioimmunoassays were developed, enabling consolidation and detailing of these early observations, and allowing explorations at the tissue level. As another aspect of the endocrine paradigm, in vivo effects of IGFs were studied. The initial demonstration of an effect of crude preparations on longitudinal growth in experimental animals raised heavy scepticism, since the effect might have been an artefact caused by contaminants. It took confirmation with highly purified preparations and biosynthetic IGF-I to ease this concern. Still, not until recent years it was demonstrated, by knocking out the genes, that a true physiological and not a pharmacological effect had been induced previously.When it was found that most tissues produce SMs and are sensitive to their actions, the concept emerged that IGFs may have para- and autocrine fu...

show abstract

“…The partial restoration of SM-C/IGF-I levels in diabetic rats following adrenalectomy indicates an adrenal component also in the regulation of this peptide, while the failure of adrenalectomy to cause complete reversal of SM-C/IGF-I levels (or of GH receptors) suggests an additional suppressive factor, perhaps related to the relative nutritional deficiency of diabetic rats [21]. One regulatory factor known to affect both receptor types and SM-C/IGF-I is GH itself.…”

Section: Discussionmentioning

confidence: 99%

“…One regulatory factor known to affect both receptor types and SM-C/IGF-I is GH itself. GH secretion is decreased in both fasting [22] and diabetes [23], conditions where hepatic GH and PRL receptors, and serum SM-C/IGF-I levels [4,21,24], are diminished. Our results could be explained if an adrenal factor, perhaps a catecholamine, were found to be a physiological regulator of pituitary GH secretion.…”

Section: Discussionmentioning

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

View full text Add to dashboard Cite

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.

show abstract

The effect of fasting on liver receptors for prolactin and growth hormone

Cited by 91 publications

References 21 publications

Plasma and Pituitary Content of Growth Hormone Luteinizing Hormone, and Prolactin in Uremic Rats

Plasma and Pituitary Content of Growth Hormone Luteinizing Hormone, and Prolactin in Uremic Rats

A Personal View on the Early History of the Insulin-Like Growth Factors

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

Contact Info

Product

Resources

About