Rise In Plasma Growth Hormone Levels Research Articles

Immunological and physiological validation of an enzyme-linked immunosorbent assay (ELISA) for the measurement of growth hormone in goat (Capra hircus) plasma

The current study describes the optimization and validation of an enzyme-linked immunosorbent assay (ELISA) for the quantification of growth hormone (GH) in blood plasma of goats, Capra hircus. A microtiter plate based competitive assay was developed using a capture ELISA for anti-ovine GH and biotinylated ovine GH. Ovine GH standards were prepared in charcoal–dextran stripped goat plasma. The assay was optimized in terms of sensitivity, specificity and precision. The sensitivity of the assay was 50pg GH/100μl, which corresponds to 0.5ng/ml plasma. A dose–response inhibition curve resulting from serially diluted goat plasma was parallel to the standard curve using ovine GH and thus it confirmed the similar specificity of ovine GH standard and endogenous GH in goat plasma for ovine GH antibody. The precision of the assay, i.e., the intra- and inter-assay coefficients of variations (for repeatability and reproducibility, respectively) for the pooled plasma samples containing two GH concentrations (32 and 2ng/ml) were 6.72%, 11.2%, 7.1% and 12.8%, respectively. To physiologically validate the assay, goats were treated with human growth hormone-releasing factor (hGRF) and there was an immediate rise in plasma GH levels in hGRF-treated goats. This ELISA is economic, safe, quick (requires only 48h), convenient and the first competitive enzyme immunoassay described for caprine GH.

Studies of Growth Hormone Secretion in Calorically Restricted Dogs: Effect of Cholinergic Agonists and Antagonists, Glucose and Thyrotropin-Releasing Hormone

The effect of caloric restriction (CR) on the growth hormone (GH) response to compounds reportedly capable of acting via somatostatinergic influences, i.e. cholinergic agonist or antagonist drug, glucose or thyrotropin-releasing hormone (TRH), administered alone or combined with GH-releasing hormone (GHRH), was evaluated in dogs. Eight beagle dogs, aged 4-5 years, underwent a 26-day period of increasing CR; they were evaluated either under basal conditions or starting from day 13 of CR, according to a schedule which allowed the mean length of CR to be similar among individual tests. CR resulted in a significant increase in basal GH levels, and starting from day 13 in a significant decrease in plasma somatomedin C levels; plasma glucose levels were significantly diminished on day 13 of CR and then remained unaltered. Administration of GHRH (GHRH1-44, 2 micrograms/kg, i.v.) induced a rise in plasma GH levels strikingly higher during CR than under basal conditions. Pyridostigmine (2 mg/kg orally), a muscarinic cholinergic agonist reportedly capable of restraining hypothalamic release of somatostatin (SS), enhanced the GH response to GHRH under basal conditions, but failed to do so during CR. Conversely, pirenzepine (0.6 mg/kg, i.v.), a muscarinic cholinergic antagonist, abolished the GHRH-induced GH rise under basal conditions, but only reduced it during CR. Only by doubling the dose of pirenzepine was complete inhibition of the GHRH-induced GH rise effected. Glucose alone (2 g/kg, p.o.) failed to modify basal GH secretion either before or during CR, but significantly inhibited the GHRH-induced GH rise either before or during CR.(ABSTRACT TRUNCATED AT 250 WORDS)

Baclofen-induced growth hormone secretion is blunted in chronic schizophrenics: Neuroendocrine evidence for a GABA disturbance in schizophrenia

To substantiate a previously reported disturbance of γ-aminobutyric acid (GABA) in chronic schizophrenia, plasma growth hormone (GH) response to a direct GABA agonist (baclofen, 10 mg) was assessed in 12 unmedicated chronic schizophrenic males and 10 sex- and age-matched healthy controls. Baclofen and placebo were administered orally, in a double-blind design, and blood samples were collected before and 30, 60, 90, 120, 180, and 240 min after drug or placebo administration. Baclofen induced a clear-cut rise in plasma GH levels over baseline values, but the GH increase observed in the patients was significantly smaller than that in controls. These results support the idea that GABA mechanisms may be impaired in chronic schizophrenia.

Effect of growth hormone-releasing stimuli in streptozotocin diabetic rats

The dynamics of growth hormone (GH) secretion in response to different GH secretagogues has been studied in adult freely moving male rats one month after induction of diabetes by single i.v. injection of streptozotocin (60 mg/kg). Baseline plasma GH concentrations and pituitary GH content were not different in streptozotocin-diabetic (St-D) rats and controls. Clonidine (0.15 mg/kg i.v.), an α 2-adrenergic agonist, failed to evoke GGH release in St-D rats. Substitution therapy with insulin (1 IU/100 g b.wt.daily) delivered through subcutaneously implanted minipumps, allowed re-institution of a normal GH responsiveness to clonidine. At odds with clonidine, FK 33–824 (0.1 mg/kg i.v.), a potent analog of the opioid peptide Met-enkephalin, induced a similar rise in plasma GH levels in control and St-D rats. Finally, administration of a synthetic replicate of a GH-releasing hormone of human pancreatic origin, hpGRF-40 (2.5 μg/kg i.v.) elicited a higher GH response in St-D rats than in controls. These data indicate that in St-D rats: (1) an impaired function of noradrenergic pathways controlling GH release is present; (2) contrary to previous beliefs, an α 2-adrenergic mechanism is not involved in the GH-releasing effect of opioid peptides; and (3) pituitary GH responsiveness to hpGRF is increased.

Administration of antisomatostatin serum to rats reverses the inhibition of pulsatile growth hormone secretion produced by injection of metergoline but not yohimbine.

We attempted to determine whether release of endogenous somatostatin (SS) in rats might mediate the apparent inhibition of growth hormone (GH) secretion produced by metergoline of yohimbine injection. Plasma GH levels in adult male rats bearing chronic right-atrial cannulae were measured at 15-min intervals during a 4-hour period around the onset of the daily dark period. Plasma GH levels in control rats (vehicle-injected) rose rapidly from low levels (< 10 ng/ml) just before darkness to very high levels (> 300 ng/ml) around the onset of the dark period, then declined to low values within 2 h. Injection of the serotonin receptor antagonist metergoline (5 mg/kg) or the adrenergic blocker yohimbine (10 mg/kg) 2.25 h before darkness significantly suppressed the subsequent rise in plasma GH levels. The effect of metergoline, but not yohimbine, on plasma GH was markedly reversed when animals were injected intravenously with anti-SS serum (0.5 ml) 1 h after drug administration. These data suggest that circulating SS may mediate the GH inhibition produced by injection of a serotonin receptor blocker; however, other factors are apparently involved in the suppression of GH secretion by yohimbine.

Inhibitory effect of somatostatin (SRIF) on the release of growth hormone (GH) induced in the rat by electrical stimulation.

The effect of synthetic SRIF on GH release induced by hypothalamic ventromedial (VMN) and basolateral amygdaloid (BLA) electrical stimulation has been investigated in rats anesthetized by pentobarbital. SRIF administered as an intravenous infusion during stimulation (500 μg/rat) or subcutaneously 5 min before stimulation (20 μg/100 g body wt) completely blocked the 4-5-fold rise in plasma GH levels which occurred after VMN stimulation. A smaller single intravenous dose of SRIF (10 μg/100 g body wt) was effective in preventing VMN-induced release when administered at the end of stimulation but not when given immediately before stimulation. SRIF (20 μg/100 g body wt sc) was also effective in blocking BLA-induced GH release. These results indicate that SRIF is active in preventing acute GH release induced by stimulation of either brain region and suggest that the site of blockade is at the pituitary level. (Endocrinology 94: 497, 1974)

Plasma growth hormone (GH) response to hypothalamic or extrahypothalamic electric stimulation.

Plasma growth hormone (GH) responses, as measured by radioimmunoassy, were determined in individual rats following electrical stimulation of various hypothalamic and extrahypothalamic sites. In the hypothalamus, positive GH responses (rise in plasma GH levels > 10 μg/ml within IS min) occurred only with stimulation of the ventromedial or arcuate nucleus. Effective extrahypothalamic stimulation sites included the hippocampus, basolateral amygdala and mesencephalic interpeduncular nucleus. Reserpine administration (5 mg/kg; 24 hr before stimulation) was effective in preventing GH release induced by hippocampal stimulation but had no effect on ventromedial—arcuate—induced GH release. These results suggest that GH release may be induced by electrical stimulation either of the “final common pathway” in the medial basal hypothalamus or of certain extrahypothalamic structures with known connections to this region. (Endocrinology 91: 107, 1972)