The effect of growth hormone on the metabolism of a tryptophan load in the liver and brain of hypophysectomized rats

1979 ◽  
Vol 57 (6) ◽  
pp. 517-522 ◽  
Author(s):  
Simon N. Young ◽  
Michael Oravec
Keyword(s):  
Growth Hormone ◽  
Psychiatric Disorders ◽  
Tyrosine Aminotransferase ◽  
Clinical Use ◽  
Hypophysectomized Rats ◽  
Tryptophan Catabolism ◽  
Tryptophan Pyrrolase ◽  
Tryptophan Content ◽  
The Brain

Growth hormone antagonizes the induction of tryptophan pyrrolase and tyrosine aminotransferase by cortisol. We have shown that, contrary to previous reports, growth hormone is also capable of antagonizing the induction of these enzymes by tryptophan and α-methyl tryptophan. As α-methyl tryptophan is not metabolized appreciably in the rat, our data show that growth hormone does not act indirectly through changes in the liver tryptophan content as was suggested previously. Growth hormone decreases the rate of tryptophan catabolism in vivo after induction of tryptophan pyrrolase by tryptophan and α-methyl tryptophan. Because the rate of catabolism of a tryptophan load is slower in animals treated with growth hormone, tissue tryptophan levels and the rate of synthesis of 5-hydroxytryptamine in the brain are higher in these animals than in those receiving tryptophan alone. Thus, although tryptophan administration raises brain 5-hydroxytryptamine levels, induction of tryptophan pyrrolase in the liver, by the load, limits the extent and duration of the rise in brain 5-hydroxytryptamine synthesis. This has important implications for the clinical use of tryptophan in psychiatric disorders, where tryptophan is given to produce long-lasting elevations of brain 5-hydroxytryptamine.

Reduced and S-carboxymethylated human growth hormone: a probe for diabetogenic action

1984 ◽  
Vol 247 (5) ◽  
pp. E639-E644
Author(s):  
C. M. Cameron ◽  
J. L. Kostyo ◽  
J. A. Rillema ◽  
S. E. Gennick
Keyword(s):  
Growth Hormone ◽  
Amino Acid ◽  
Human Growth Hormone ◽  
Human Growth ◽  
Mouse Mammary Gland ◽  
Amino Acid Incorporation ◽  
Acid Incorporation ◽  
Hypophysectomized Rats

The biological activity profile of reduced and S-carboxymethylated human growth hormone (RCM-hGH) was determined to establish its suitability for study of the diabetogenic property of hGH. RCM-hGH was found to have greatly attenuated in vivo growth-promoting activity in the 9-day weight-gain test in hypophysectomized rats (approximately 1%) and to have a similar low order of in vitro activity in stimulating amino acid incorporation into the protein of the isolated rat diaphragm. RCM-hGH also only had approximately 1% of the in vitro insulin-like activity of the native hormone on isolated adipose tissue from hypophysectomized rats. In contrast, RCM-hGH retained substantial in vivo diabetogenic activity in the ob/ob mouse, appearing to have approximately 50% of the activity of the native hormone. RCM-hGH was also found to retain significant, although attenuated (25%), in vitro lactogenic activity when tested for the ability to stimulate amino acid incorporation into a casein-rich protein fraction in mouse mammary gland explants. Because RCM-hGH exhibits a high degree of diabetogenic activity, although lacking significant anabolic or insulin-like activities, it will be useful as a "monovalent" probe for the study of the molecular mechanism of the diabetogenic action of GH.

IN VITRO AND IN VIVO EFFECT OF GROWTH HORMONE ON ALDOSTERONE SECRETION

1960 ◽  
Vol 38 (1) ◽  
pp. 1069-1075
Author(s):  
O. J. Lucis ◽  
E. H. Venning
Keyword(s):  
Growth Hormone ◽  
Adrenal Gland ◽  
Human Growth Hormone ◽  
Human Growth ◽  
Secretion Rate ◽  
Aldosterone Secretion ◽  
Hypophysectomized Rats

Porcine, monkey, and human growth hormone have no effect on the in vitro secretion of aldosterone by the rat adrenal gland. When monkey growth hormone is injected into hypophysectomized rats, the adrenals of these animals secrete, under in vitro conditions, increased amounts of aldosterone with no change in the secretion rate of corticosterone. The plasma of these rats contains a substance which appears to stimulate the secretion of aldosterone in the adrenals of normal rats.

scholarly journals Interactions of ghrelin signaling pathways with the GH neuroendocrine axis: a new and experimentally tested model

2009 ◽  
Vol 43 (3) ◽  
pp. 105-119 ◽  
Author(s):  
Clemens Wagner ◽  
S Roy Caplan ◽  
Gloria S Tannenbaum
Keyword(s):  
Growth Hormone ◽  
Vagus Nerve ◽  
Present Model ◽  
Male Rat ◽  
Extended Model ◽  
Growth Hormone Releasing Hormone ◽  
Hypothalamic Neuropeptides ◽  
Neuroendocrine Axis ◽  
The Brain

Growth hormone (GH) is secreted in a pulsatile fashion from the pituitary gland into the circulation. Release is governed by two hypothalamic neuropeptides, growth hormone-releasing hormone (GHRH) and somatostatin (SRIF), resulting in secretion episodes with a periodicity of 3.3 h in the male rat. Ghrelin is an additional recently identified potent GH-secretagogue. However, its in vivo interactions with the GH neuroendocrine axis remain to be elucidated. Moreover, two different sites of ghrelin synthesis are involved, the stomach and the hypothalamus. We used our previously developed core model of GH oscillations and added the sites of ghrelin action at the pituitary and in the hypothalamus. With this extended model, we simulated the effects of central and peripheral ghrelin injections, monitored the GH profile and compared it with existing experimental results. Systemically administered ghrelin elicits a GH pulse independent of SRIF, but only in the presence of GHRH. The peripheral ghrelin signal is mediated to the brain via the vagus nerve, where it augments the release of GHRH and stimulates the secretion of neuropeptide-Y (NPY). By contrast, centrally administered ghrelin initiates a GH pulse by increasing the GHRH level and by antagonizing the SRIF block at the pituitary. In addition, NPY neurons are activated, which trigger a delayed SRIF surge. The major novel features of the present model are a) the role played by NPY, and b) the dissimilar functions of ghrelin in the hypothalamus and at the pituitary. Furthermore, the predictions of the model were experimentally examined and confirmed.

A new bioassay for human growth hormone based on incorporation of labelled proline into skin

1982 ◽  
Vol 95 (1) ◽  
pp. 81-86 ◽  
Author(s):  
C. G. Rudman ◽  
Rose E. Gaines Das ◽  
J. A. Parsons
Keyword(s):  
Growth Hormone ◽  
Weight Gain ◽  
Human Growth Hormone ◽  
Dose Response ◽  
Human Growth ◽  
Hypophysectomized Rats ◽  
In Vivo Bioassay ◽  
New Bioassay ◽  
Average Index

An in-vivo bioassay for human growth hormone (hGH) has been developed, based on the dose-related enhancement of radioactivity in skin of hypophysectomized rats given daily s.c. injections of hGH and a single i.p. injection of labelled proline. The measured radioactivity, taken as the response, was shown to be independent of the site at which the skin was sampled. Valid dose–response relationships were obtained after as little as 3 days of treatment with GH. The assays by this method are shown to be more precise than the widely used weight-gain and tibial-width bioassays. Assays carried out gave an average index of precision of 0·036.

Active transport of calcium by intestine: effects of hypophysectomy and growth hormone

1962 ◽  
Vol 203 (5) ◽  
pp. 873-880 ◽  
Author(s):  
James D. Finkelstein ◽  
David Schachter
Keyword(s):  
Growth Hormone ◽  
Active Transport ◽  
Electrical Potential ◽  
Potential Gradient ◽  
Initial Increase ◽  
Bovine Growth Hormone ◽  
Hypophysectomized Rats ◽  
Rat Duodenum

The effects of hypophysectomy on active transport of calcium in vitro by everted gut sacs of rat duodenum are 1) an initial increase 4–5 days postoperatively and 2) a marked decrease 2–3 weeks postoperatively. The defect in transport results from reduction in the unidirectional transfers of Ca toward the serosa, and both steps in the transport (mucosal uptake and transfer to serosal surface) are impaired. Hypophysectomy also decreases iron transport (duodenal gut sacs), decreases l-proline transfer less strikingly (ileal gut sacs), increases d-galactose transport (jejunal gut sacs), and does not appear to influence either the electrical potential gradient from mucosa to serosa or the net flux of sodium. Treatment of hypophysectomized rats with a preparation of bovine growth hormone restores transfer mechanisms for calcium and iron. Ovine prolactin is also active in restoring the Ca mechanism, whereas other pituitary and nonpituitary hormones are not. Cortisone, l-thyroxin, and estradiol decrease Ca transport further in hypophysectomized rats. Absorption of Ca from loops of rat duodenum in vivo is also decreased 2 weeks after hypophysectomy and can be increased by prior treatment with bovine growth hormone.

IN VITRO AND IN VIVO EFFECT OF GROWTH HORMONE ON ALDOSTERONE SECRETION

1960 ◽  
Vol 38 (10) ◽  
pp. 1069-1075 ◽  
Author(s):  
O. J. Lucis ◽  
E. H. Venning
Keyword(s):  
Growth Hormone ◽  
Adrenal Gland ◽  
Human Growth Hormone ◽  
Human Growth ◽  
Secretion Rate ◽  
Aldosterone Secretion ◽  
Hypophysectomized Rats

Porcine, monkey, and human growth hormone have no effect on the in vitro secretion of aldosterone by the rat adrenal gland. When monkey growth hormone is injected into hypophysectomized rats, the adrenals of these animals secrete, under in vitro conditions, increased amounts of aldosterone with no change in the secretion rate of corticosterone. The plasma of these rats contains a substance which appears to stimulate the secretion of aldosterone in the adrenals of normal rats.

scholarly journals Retinal correlates of psychiatric disorders

2020 ◽  
Vol 11 ◽  
pp. 204062232090521 ◽  
Author(s):  
Melanie T. Almonte ◽  
Pamela Capellàn ◽  
Timothy E. Yap ◽  
Maria Francesca Cordeiro
Keyword(s):  
Psychiatric Disorders ◽  
Clinical Symptoms ◽  
Brain Dysfunction ◽  
Microscopic Level ◽  
Robust Methods ◽  
Functional Changes ◽  
Self Reports ◽  
Progression Of Disease ◽  
The Brain

Diagnosis and monitoring of psychiatric disorders rely heavily on subjective self-reports of clinical symptoms, which are complicated by the varying consistency of accounts reported by patients with an impaired mental state. Hence, more objective and quantifiable measures have been sought to provide clinicians with more robust methods to evaluate symptomology and track progression of disease in response to treatments. Owing to the shared origins of the retina and the brain, it has been suggested that changes in the retina may correlate with structural and functional changes in the brain. Vast improvements in retinal imaging, namely optical coherence tomography (OCT) and electrodiagnostic technology, have made it possible to investigate the eye at a microscopic level, allowing for the investigation of potential biomarkers in vivo. This review provides a summary of retinal biomarkers associated with schizophrenia, bipolar disorder and major depression, demonstrating how retinal biomarkers may be used to complement existing methods and provide structural markers of pathophysiological mechanisms that underpin brain dysfunction in psychiatric disorders.

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