scholarly journals 295 Awardee Talk: Novel regulation of growth hormone by kisspeptin

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 136-136
Author(s):  
James Sartin ◽  
Jay A Daniel ◽  
Chad Foradori ◽  
Brian Whitlock
Keyword(s):  
Growth Hormone ◽  
Arcuate Nucleus ◽  
Reproductive Function ◽  
Releasing Hormone ◽  
Npy Receptor ◽  
Ghrelin Receptors ◽  
Critical Requirement ◽  
Plasma Gh ◽  
Regulation Of Growth ◽  
Stimulation Of

Abstract Kisspeptin (KP) is critical regulator of reproductive function through it’s potent stimulation of gonadotropin releasing hormone (GnRH). In addition there has been inconclusive evidence to suggest intravenous KP can stimulate growth hormone (GH). Studies in 24 h fasted (but not fed) sheep determined that ICV injection of Kp-10 can increase plasma GH concentrations. This led to questions about the mechanism linking KP and GH. Since fasting is a critical requirement for the Kp effect on GH, studies were focused on factors that are linked to fasting within the hypothalamus and are known regulators of GH. Fasting causes a major upregulation of neuropeptide Y (NPY), a potent appetite regulator and in ruminants, a stimulator of GH. Pretreatment of BIBO 3304, an NPY receptor antagonist, blocked the effect of KP to increase GH and implicated NPY as a mediator of the KP effect. Indeed, KP injected ICV upregulated cFOS in NPY and GH Releasing Hormone (GHRH) cells in the arcuate nucleus and reduced cFOS in Somatostatin (SS) cells in the periventricular nucleus. Another factor, altered by fasting and capable of regulating GH, is Ghrelin. Both blockage of Ghrelin release and central blockade of Ghrelin receptors reduced or blocked release of GH after KP treatment. These experiments suggest an hypothesis that fasting upregulates central Ghrelin and NPY expression permitting the activation of NPY by KP. NPY in turn activates GHRH and inhibits SS to release GH.

scholarly journals Ghrelin Stimulation of Growth Hormone-Releasing Hormone Neurons Is Direct in the Arcuate Nucleus

PLoS ONE ◽  
2010 ◽  
Vol 5 (2) ◽  
pp. e9159 ◽  
Author(s):  
Guillaume Osterstock ◽  
Pauline Escobar ◽  
Violeta Mitutsova ◽  
Laurie-Anne Gouty-Colomer ◽  
Pierre Fontanaud ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Arcuate Nucleus ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Stimulation Of

Neuroanatomic localization of the inhibitory effect of TRH on growth hormone secretion

1987 ◽  
Vol 253 (4) ◽  
pp. E354-E359
Author(s):  
K. Ishikawa ◽  
H. Katakami ◽  
L. A. Frohman
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Inhibitory Effect ◽  
Releasing Hormone ◽  
Hypothalamic Deafferentation ◽  
Electrolytic Lesions ◽  
Plasma Gh ◽  
The Right ◽  
Lateral Cerebral Ventricle

The inhibitory effect of centrally administered thyrotropin-releasing hormone (TRH) on the plasma growth hormone (GH) response to GH-releasing hormone (GHRH) in the rat was studied in relation to the anatomic loci involved. Experiments were performed in animals with bilateral electrolytic lesions in the medial preoptic (MPO) area or with anterolateral hypothalamic deafferentation and in sham-operated controls. Blood samples were obtained every 10 to 20 min from and drugs were injected into freely moving animals with indwelling cannulas in the right atrium and lateral cerebral ventricle. In control animals, the plasma GH response to GHRH, 1 microgram iv, was almost completely inhibited by TRH, 1 microgram icv, injected 5 min previously. In animals with either MPO lesions or anterolateral hypothalamic deafferentation in which median eminence somatostatin immunochemical staining was almost completely eliminated, the GH response to GHRH was enhanced and TRH did not exhibit any inhibitory effect. These results, together with the previous observation that the inhibitory effect of TRH is blocked by prior treatment with anti-somatostatin serum, suggest that the effect of TRH is mediated by stimulation of somatostatin-containing neurons in the periventricular nucleus of the MPO area.

scholarly journals Pre- and posthatch developmental changes in hypothalamic thyrotropin-releasing hormone and somatostatin concentrations and in circulating growth hormone and thyrotropin levels in the chicken

1998 ◽  
Vol 159 (2) ◽  
pp. 219-225 ◽  
Author(s):  
KL Geris ◽  
LR Berghman ◽  
ER Kuhn ◽  
VM Darras
Keyword(s):  
Growth Hormone ◽  
Embryonic Development ◽  
Present Report ◽  
Thyrotropin Releasing Hormone ◽  
The Other ◽  
Developmental Changes ◽  
Releasing Hormone ◽  
Steep Increase ◽  
Plasma Gh ◽  
Tsh Levels

Thyrotropin-releasing hormone (TRH) and somatostatin (SRIH) concentrations were determined by RIA during both embryonic development and posthatch growth of the chicken. Both TRH and SRIH were already detectable in hypothalami of 14-day-old embryos (E14). Towards the end of incubation, hypothalamic TRH levels increased progressively, followed by a further increase in newly hatched fowl. SRIH concentrations remained stable from E14 to E17 and doubled between E17 and E18 to a concentration which was observed up to hatching. Plasma GH levels remained low during embryonic development, ending in a steep increase at hatching. Plasma TSH levels on the other hand decreased during the last week of the incubation. During growth, TRH concentrations further increased, whereas SRIH concentrations fell progressively towards those of adult animals. Plasma TSH levels increased threefold up to adulthood; the rise in plasma GH levels during growth was followed by a drop in adults. In conclusion, the present report shows that important changes occur in the hypothalamic TRH and SRIH concentration during both embryonic development and posthatch growth of the chicken. Since TRH and SRIH control GH and TSH release in the chicken, the hypothalamic data are compared with plasma GH and TSH fluctuations.

Thyrotrophin and prolactin responses to thyrotrophin-releasing hormone in patients with Parkinson's disease

1982 ◽  
Vol 99 (3) ◽  
pp. 344-351 ◽  
Author(s):  
Abraham Martinez-Campos ◽  
Paolo Giovannini ◽  
Antonello Novelli ◽  
Daniela Cocchi ◽  
Tommaso Caraceni ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Growth Hormone ◽  
Parkinson's Disease ◽  
Chronic Treatment ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Marked Diminution ◽  
Dopaminergic Tone ◽  
Plasma Gh

Abstract. The thyrotrophin (TSH) and prolactin (Prl)-releasing effects of TSH-releasing hormone (TRH) were investigated in 20 subjects with Parkinson's disease (PD), unmedicated, on chronic treatment with a combination levodopa-benserazide (Madopar) or levodopa-carbidopa (Sinemet) or withdrawn from therapy. Administration of TRH (200 μg iv) induced in unmedicated patients TSH and Prl responses significantly lower than those of sex-and age-matched controls. In patients on Madopar therapy the TSH and Prl responses to TRH were greater than in unmedicated patients and comparable to those of controls, while in patients on Sinemet therapy the pituitary responses were undistinguishable from those of unmedicated subjects. Withdrawal of Madopar therapy resulted in a marked diminution of the TSH response but did not affect the Prl response to TRH. Withdrawal of Sinemet therapy did not alter the TSH and Prl responses to TRH. Concomitant evaluation of growth hormone (GH) levels, in none of the subjects evidenced non-specific changes in plasma GH following TRH. Since TSH and Prl responses to TRH are inhibited by an enhancement of the dopaminergic tone, it would appear that the latter is preserved in the tuberoinfundibular system of unmedicated subjects and subjects on chronic Sinemet therapy, but is defective in subjects on chronic Madopar therapy.

Sign in / Sign up

Export Citation Format

Share Document