A Receptor in Pituitary and Hypothalamus That Functions in Growth Hormone Release

Howard, Andrew D.; Feighner, Scott D.; Cully, Doris; Arena, Joseph P.; Liberator, Paul; Rosenblum, Charles; Hamelin, Michel; Hreniuk, Donna L.; Palyha, Oksana; Anderson, Jennifer W.; Paress, Philip S.; Dı́az, Carmen; Chou, Michael F.; Liu, Ken K.; McKee, Karen K.; Pong, Sheng-Shung; Chaung, L Y; Elbrecht, Alex; Dashkevicz, Mike; Heavens, R.P.; Rigby, Michael; Sirinathsinghji, D.J.S.; Dean, Dennis C.; Melillo, David G.; Patchett, Arthur A.; Nargund, Ravi P.; Griffin, Patrick R.; DeMartino, Julie A.; Gupta, Sunil; Schaeffer, James M.; Smith, Roy G.; Ploeg, Lex H.T. Van der

doi:10.1126/science.273.5277.974

Cited by 1,926 publications

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“…GHS receptor could not be detected in the thymus (13), and GHS does not affect proliferation of T or B cells in vitro (our unpublished observation). However, lymphoid cells are known to have GH receptors, which may contribute to the immune enhancing effect (1-3).…”

Section: Discussionmentioning

confidence: 99%

“…The release of GH is similar to physiological release of GH in that it is under pulsating regimen and is subjected to feedback mechanism (11). In vitro experiments showed that GHS promotes GH release by acting on a specific G protein-coupled receptor located in the hypothalamus and pituitary gland (13). The natural or endogenous ligand for this receptor was recently identified and it was named ghrelin (14).…”

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confidence: 99%

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Immune Enhancing Effect of a Growth Hormone Secretagogue

Koo¹,

Huang²,

Camacho³

et al. 2001

The Journal of Immunology

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104

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Growth hormone (GH) has been known to enhance immune responses, whether directly or through the insulin like growth factor-1, induced by GH. Recently a nonpeptidyl small m.w. compound, a GH secretagogue (GHS), was found to induce the production of GH by the pituitary gland. In this study, we examined the effect of GHS in immunological functions of 5- to 6-wk-old and 16- to 24-month-old mice. In young mice, we observed a significant increase in PBLs, but T and B cell-proliferative responses were not consistently enhanced. The old mice, treated with GHS for 3 wk, did not show increases in peripheral lymphocytes, but they exhibited a statistically significant increase in thymic cellularity and differentiation. When inoculated with a transplantable lymphoma cell line, EL4, the treated old mice showed statistically significant resistance to the initiation of tumors and the subsequent metastases. Generation of CTL to EL4 cells was also enhanced in the treated mice, suggesting that GHS has a considerable immune enhancing effect, particularly in the old mice. We have also found that GHS promoted better thymic engraftment in bone marrow transplant of SCID mice. We found more cycling cells in the spleens of treated mice, suggesting that GHS may exert its immune enhancing effect by promoting cell division in lymphoid cells. These observations ascribe to GHS a novel therapy possible for aging, AIDS, and transplant individuals, whose immune functions are compromised.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Immune Enhancing Effect of a Growth Hormone Secretagogue

Koo¹,

Huang²,

Camacho³

et al. 2001

The Journal of Immunology

Self Cite

104

View full text Add to dashboard Cite

show abstract

“…Mammalian GHS-R gene is composed of two exons, and two types of GHS-R mRNAs, GHS-R1a and 1b, are generated by alternative transcription process of the gene (Howard et al, 1996). So far, GHS-Rs have been identified in mammals (Howard et al, 1996;Katayama et al, 2000;Kitazawa et al, 2011;Suzuki et al, 2012), avians (Geelissen et al, 2003;Tanaka et al, 2003) and several fish species (Palyha et al, 2000;Chan and Cheng, 2004;Olsson et al, 2008;Kaiya et al, 2009a,b;Small et al, 2009;Eom et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Sequence, genomic organization and expression of ghrelin receptor in grass carp, Ctenopharyngodon idellus

Cai

Yuan

et al. 2015

Comparative Biochemistry and Physiology Part A: Molecular &

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“…Although UnAG signaling/receptor interactions remain largely unknown, classical ghrelin signaling via GHS‐R1a results in the transient release of calcium (Howard et al. 1996; Kojima et al. 1999).…”

Section: Resultsmentioning

confidence: 99%

Acylated and unacylated ghrelin do not directly stimulate glucose transport in isolated rodent skeletal muscle

Cervone

Dyck

2017

Physiol Rep

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Emerging evidence implicates ghrelin, a gut‐derived, orexigenic hormone, as a potential mediator of insulin‐responsive peripheral tissue metabolism. However, in vitro and in vivo studies assessing ghrelin's direct influence on metabolism have been controversial, particularly due to confounding factors such as the secondary rise in growth hormone (GH) after ghrelin injection. Skeletal muscle is important in the insulin‐stimulated clearance of glucose, and ghrelin's exponential rise prior to a meal could potentially facilitate this. This study was aimed at elucidating any direct stimulatory action that ghrelin may have on glucose transport and insulin signaling in isolated rat skeletal muscle, in the absence of confounding secondary factors. Oxidative soleus and glycolytic extensor digitorum longus skeletal muscles were isolated from male Sprague Dawley rats in the fed state and incubated with various concentrations of acylated and unacylated ghrelin in the presence or absence of insulin. Ghrelin did not stimulate glucose transport in either muscle type, with or without insulin. Moreover, GH had no acute, direct stimulatory effect on either basal or insulin‐stimulated muscle glucose transport. In agreement with the lack of observed effect on glucose transport, ghrelin and GH also had no stimulatory effect on Ser473 AKT or Thr172 AMPK phosphorylation, two key signaling proteins involved in glucose transport. Furthermore, to our knowledge, we are among the first to show that ghrelin can act independent of its receptor and cause an increase in calmodulin‐dependent protein kinase 2 (CaMKII) phosphorylation in glycolytic muscle, although this was not associated with an increase in glucose transport. We conclude that both acylated and unacylated ghrelin have no direct, acute influence on skeletal muscle glucose transport. Furthermore, the immediate rise in GH in response to ghrelin also does not appear to directly stimulate glucose transport in muscle.

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A Receptor in Pituitary and Hypothalamus That Functions in Growth Hormone Release

Cited by 1,926 publications

References 19 publications

Immune Enhancing Effect of a Growth Hormone Secretagogue

Immune Enhancing Effect of a Growth Hormone Secretagogue

Sequence, genomic organization and expression of ghrelin receptor in grass carp, Ctenopharyngodon idellus

Acylated and unacylated ghrelin do not directly stimulate glucose transport in isolated rodent skeletal muscle

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