Long-Term Failure of Compensatory Growth in Rats following Acute Neonatal Passive Immunization against Growth Hormone-Releasing Hormone

Wehrenberg, William B.; Voltz, Donald M.; Cella, Silvano G.; Müller, Eugenio E.; Gaillard, Rolf C.

doi:10.1159/000126268

Cited by 15 publications

(4 citation statements)

References 16 publications

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“…The changes in serum IGF-I indi¬ cated that significant changes in serum GH levels were being achieved, as found previously using this antiserum and GH therapy regime (Flint & Gardner 1993, Vernon et al 1993, Doris et al 1994. Furthermore, we have previously shown that administration of our anti-rGH inhibits growth in rats (Flint & Gardner 1993); this is consistent with other studies which have demonstrated that serum GH levels can be lowered by treatment of rats with antisera against GH-releasing hormone (Tannenbaum & Ling 1984, Wehrenberg et al 1992, resulting in inhibition of growth. The reduction in serum insulin levels induced by immunoneutralisation of serum GH was consistent with previous observations and may be attributable to the decrease in food intake which occurs as a consequence of anti-rGH treatment (Palmer et al 1993).…”

Section: Discussionsupporting

confidence: 89%

Divergent regulation of rat adipocyte GLUT1 and GLUT4 glucose transporters by GH

Kilgour

Baldwin²,

Flint³

1995

Journal of Endocrinology

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The effect of GH, in vivo, on the glucose transport systems of rat adipocytes has been investigated. Lowering of serum GH levels, by treatment of rats with an antiserum specific for rat GH (anti-rGH), significantly decreased serum levels of both IGF-I and insulin. Treatment with anti-rGH also increased glucose oxidation and the conversion of glucose to lipid by isolated adipocytes. Adipocyte glucose oxidation and lipid synthesis were measured in the presence of a limiting concentration of glucose and therefore reflect changes in glucose transport. Immunoblot analysis of adipocyte subcellular fractions revealed that anti-rGH induced an increase in the amount of the glucose transporters GLUT1 (1\m=.\6-fold) and GLUT4 (2\m=.\5-fold)present in plasma membranes and a decrease (39%) in the amount of GLUT4 present in low-density microsomal fractions. Lowering of serum GH also increased, by 36%, the amount of GLUT1 present in a total membrane fraction but had no such effect on GLUT4 levels. Replenishment of serum GH, by concurrent administration of ovine GH to rats, prevented all of these effects of anti-rGH. It was concluded that GH in vivo down-regulates the amount of both GLUT1 and GLUT4 present in rat adipocyte plasma membranes. This reflects a decrease in the total cellular levels of GLUT1 and modification of the subcellular distribution of GLUT4 and results in restriction of adipocyte glucose uptake.

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Section: Discussionsupporting

confidence: 89%

Divergent regulation of rat adipocyte GLUT1 and GLUT4 glucose transporters by GH

Kilgour

Baldwin²,

Flint³

1995

Journal of Endocrinology

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“…The aim of the present study was to investigate the effects of 3-to 10-day treatment with Hexarelin on GH release and GH mRNA levels in infant and young-adult rats passively immunized against GHRH, an experimen tal condition of impaired somatotropic function [20][21][22],…”

Section: Introductionmentioning

confidence: 99%

Hexarelin Stimulation of Growth Hormone Release and mRNA Levels in an Infant and Adult Rat Model of Impaired GHRH Function

Torsello

Luoni²,

Grilli³

et al. 1997

Neuroendocrinology

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Hexarelin, a GH-releasing peptide, is an effective GH secretagogue in man and a variety of experimental animals. In the present study, we sought to characterize the effects of short-term Hexarelin treatment on GH release and GH mRNA levels in infant and young-adult rats and in rats of either age passively immunized with an antiserum against GHRH (GHRH-Ab). Hexarelin (80 µg/ kg, b.i.d. s.c), administered for 3, 5 or 10 days to 8-, 6- and 1-day-old rats, respectively, induced a progressive enhancement of the plasma GH rise elicited by a subsequent acute Hexarelin (80 µg/kg s.c.) challenge when pups were 10 days old. As expected, GHRH-Ab treatment decreased GH concentrations in 10-day-old pups. In GHRH-Ab-treated pups, Hexarelin administration for 3-10 days significantly enhanced the GH response to the acute Hexarelin injection, though the mean plasma GH values remained significantly lower than in the respective control group. Hexarelin treatment did not alter GH mRNA levels in control pups. In GHRH-Ab-treated pups Hexarelin treatment for 3 and 5 days, but not 10 days, restored GH mRNA levels to control values. In young-adult male rats, regardless of antiserum treatment, Hexarelin administration for 5 or 10 days significantly suppressed the GH response to a subsequent acute challenge with the peptide. Yet, 5-10 days of Hexarelin treatment did not alter GH mRNA in control young-adult rats. In adult rats GHRH-Ab also decreased GH mRNA levels, but 10 days of Hexarelin treatment were necessary to return GH mRNA back to normal levels. These results indicate that: (1) the effects of Hexarelin on GH release and GH mRNA levels may be unrelated events; (2) deprivation of GHRH function discloses the ability of Hexarelin to stimulate GH mRNA levels; (3) age plays a crucial role in setting the pituitary responsiveness to short-term Hexarelin treatment, and (4) the different ability of Hexarelin to stimulate GH release and GH synthesis in neonatal and young-adult rats may have clinical relevance in the chronic administration of the peptide.

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“…When GHRH deprivation is induced during fetal life or during the early neonatal period, the failure of compensatory growth following treatment suggests that a functional GHRH-GH endocrine system is critical during the neonatal period to establish normal growth on a long-term basis [22, 23]. …”

Section: Role Of Ghrh In Gh Secretion and Growthmentioning

confidence: 99%

Growth Hormone-Releasing Hormone: Past and Present

Sassolas¹

2000

Horm Res Paediatr

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The discovery of hypothalamic hypophysiotropic factors confirmed the hypothesis of Green and Harris in the late 1940s. These hormones were isolated from their eutopic site of production (the hypothalamus) with the exception of growth hormone (GH)-releasing hormone (GHRH), which was isolated from an ectopic, tumoral site of production and found to be responsible for acromegaly. Following the isolation, characterization and synthesis of human GHRH, clinical studies were performed and are described below. Circulating levels of GHRH can be measured and provide the basis for the diagnosis of acromegaly related to the ectopic, tumoral production of GHRH. At present, GHRH is used as a test of GH secretion mainly as an adjunct to other agents which modify somatostatin status, or to GH-releasing peptides. Its therapeutic potential in children and the elderly is still under investigation. The role of GHRH in the pulsatile secretion of GH is described.

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Long-Term Failure of Compensatory Growth in Rats following Acute Neonatal Passive Immunization against Growth Hormone-Releasing Hormone

Cited by 15 publications

References 16 publications

Divergent regulation of rat adipocyte GLUT1 and GLUT4 glucose transporters by GH

Divergent regulation of rat adipocyte GLUT1 and GLUT4 glucose transporters by GH

Hexarelin Stimulation of Growth Hormone Release and mRNA Levels in an Infant and Adult Rat Model of Impaired GHRH Function

Growth Hormone-Releasing Hormone: Past and Present

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