Induction of Chronic Growth Hormone Deficiency by Anti-GH Serum

Grindeland, R. E.; Smith, Adolph; Evans, Edward S.; Ellis, Stanley

doi:10.1210/endo-95-3-793

Cited by 14 publications

(5 citation statements)

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“…The inhi¬ bition of growth continued after cessation of anti-(rGH) treatment, also became apparent within 24 h of cessation of GH treatment in anti-(rGH)-treated rats which received concurrent oGH injections and was still evident 4 weeks after commencing treatment. The effects on pup growth are similar to those previously reported by Grindeland, Smith, Evans & Ellis (1974) although they attributed the suppression of growth during the first 21 days of treatment to a non-specific effect of serum and they did not find any decrease in serum GH. Our results, in which GH injections over¬ came the effects of anti-(rGH), however, clearly show them to be due specifically to neutralization of GH.…”

Section: Discussionsupporting

confidence: 88%

“…Pituitary weight during the first 14 days was reduced by a mean value of 37% and GH content 45% compared with a 20% reduction in body weight, suggesting a specific effect on the pituitary. Similar findings were reported by Grindeland et al (1974). Within the pituitary gland itself GH concentration was reduced whilst prolactin concentration was increased, although neither of these changes achieved statistical significance.…”

Section: Discussionsupporting

confidence: 85%

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Inhibition of neonatal rat growth and circulating concentrations of insulin-like growth factor-I using an antiserum to rat growth hormone

Flint

Gardner²

1989

Journal of Endocrinology

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Treatment of rats for 24 h on day 2, 10 or 20 of age with a specific antiserum to rGH (anti-(rGH], GH, bromocriptine (CB-154) or prolactin failed to influence body weight gain or serum concentrations of insulin-like growth factor-I (IGF-I). On day 28 of age, however, anti-(rGH) completely inhibited body weight gain and markedly reduced circulating IGF-I concentrations, effects which were completely prevented by exogenous ovine GH (oGH). When administered to control rats on day 28 oGH caused supranormal weight gain and serum IGF-I concentrations. These results suggested that GH does not play a significant role in growth or regulation of serum IGF-I until after day 20 of age. By contrast, when anti-(rGH) was given for 4 consecutive days beginning on day 2 of life, body weight gain was reduced within 48 h and remained so until at least 28 days of age. Tail length was also significantly reduced. The effect was due to inhibition of GH effects since serum GH concentrations were low and exogenous GH prevented the effect. Inhibition of growth during the first 14 days of life occurred in the absence of any effect on serum IGF-I although by 21 days of age serum IGF-I was considerably lower than in control rats. The prolonged reduction in growth after treatment has stopped appeared to be due to a cytotoxic effect on the pituitary gland since pituitary weight and GH but not prolactin content were significantly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 85%

Inhibition of neonatal rat growth and circulating concentrations of insulin-like growth factor-I using an antiserum to rat growth hormone

Flint

Gardner²

1989

Journal of Endocrinology

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“…The results of this study confirm and extend the findings of our previous study (Flint & Gardner, 1989) as well as those of others (Grindeland, Smith, Evans & Ellis, 1974;Ellis, Vodian & Grindeland, 1978), and demonstrate that a specific antiserum to rGH can produce reductions in body weight gain and serum IGF-I lasting more than 6 weeks. How this effect is produced is unclear since circulating con¬ centrations of antibodies would not be expected to remain sufficiently potent for this length of time due to their neutralization in 7-10 days by rat antibodies against the sheep -globulin injected.…”

Section: Discussionsupporting

confidence: 92%

Long-term reductions in GH, insulin-like growth factor-I and body weight gain in rats treated neonatally with antibodies to rat GH

Gardner

Flint²

1990

Journal of Endocrinology

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Treatment of neonatal rats on days 2-5 with antibodies against rat GH (rGH) markedly reduced body weight gain and serum concentrations of insulin-like growth factor-I for 6-8 weeks in both females and males, after which weight gain normalized without evidence of catch-up growth. There were no significant effects on serum prolactin, tri-iodothyronine or corticosterone. Testis and ovarian weights were reduced, although only in proportion to body size. In females, but not males, the treated rats, though lighter, had increased fat deposition in the parametrial depot. Pituitary weight was considerably reduced over 100 days later, as was the pituitary content of GH, but not prolactin. The response to GH-releasing factor of both male and female rats was also greatly reduced at this time. Taken together with the fact that these rGH antibodies can bind directly to somatotrophs, we propose that the long-term effects of the antibodies are induced by specific somatotroph destruction.

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“…Several lines of evidence demonstrate that the tibial growth, as used in the present bioassay, is not a measure of iGH. First, tibial growth was not inhibited by systemic administration of antibodies engendered to 22-kDa pituitary GH, the antibodies used to measure iGH; this indicates that the influence of 22-kDa GH on the bioassay is minimal (9,11,15). Second, basal levels of plasma iGH in the rat…”

Section: Source and Type Of Afferents That Can Regulate Bghmentioning

confidence: 99%

Skeletal muscle afferent regulation of bioassayable growth hormone in the rat pituitary

Gosselink¹,

Grindeland

Roy

et al. 1998

Journal of Applied Physiology

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There are forms of growth hormone (GH) in the plasma and pituitary of the rat and in the plasma of humans that are undetected by presently available immunoassays (iGH) but can be measured by bioassay (bGH). Although the regulation of iGH release is well documented, the mechanism(s) of bGH release is unclear. On the basis of changes in bGH and iGH secretion in rats that had been exposed to microgravity conditions, we hypothesized that neural afferents play a role in regulating the release of these hormones. To examine whether bGH secretion can be modulated by afferent input from skeletal muscle, the proximal or distal ends of severed hindlimb fast muscle nerves were stimulated ( approximately 2 times threshold) in anesthetized rats. Plasma bGH increased approximately 250%, and pituitary bGH decreased approximately 60% after proximal nerve trunk stimulation. The bGH response was independent of muscle mass or whether the muscles were flexors or extensors. Distal nerve stimulation had little or no effect on plasma or pituitary bGH. Plasma iGH concentrations were unchanged after proximal nerve stimulation. Although there may be multiple regulatory mechanisms of bGH, the present results demonstrate that the activation of low-threshold afferents from fast skeletal muscles can play a regulatory role in the release of bGH, but not iGH, from the pituitary in anesthetized rats.

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Induction of Chronic Growth Hormone Deficiency by Anti-GH Serum

Cited by 14 publications

References 0 publications

Inhibition of neonatal rat growth and circulating concentrations of insulin-like growth factor-I using an antiserum to rat growth hormone

Inhibition of neonatal rat growth and circulating concentrations of insulin-like growth factor-I using an antiserum to rat growth hormone

Long-term reductions in GH, insulin-like growth factor-I and body weight gain in rats treated neonatally with antibodies to rat GH

Skeletal muscle afferent regulation of bioassayable growth hormone in the rat pituitary

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