Integrating GHS into the Ghrelin System

Veldhuis, Johannes D.; Bowers, Cyril Y.

doi:10.1155/2010/879503

Cited by 49 publications

(46 citation statements)

References 640 publications

(736 reference statements)

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“…There are currently two identified ghrelin receptor types, the GHS-R1a and GHS-R1b. The GHS-R1a is reported to bind ghrelin and GHS and mediate their respective actions while the 1b type is categorized as nonfunctional (Ghigo et al, 2005; Veldhuis and Bowers, 2010). Ventricular administration of ghrelin induces c-Fos expression in the PVN where GHS-R1a are localized (Lawrence et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Urocortin I inhibits the effects of ghrelin and neuropeptide Y on feeding and energy substrate utilization

et al. 2011

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The corticotropin releasing hormone-related ligand, urocortin-I (UcnI), suppresses food intake when injected into multiple hypothalamic and extrahypothalamic areas. UcnI also alters energy substrate utilization, specifically via enhanced fat oxidation as reflected in reductions in respiratory quotient (RQ). In the present study we compared the feeding and metabolic effects of ghrelin and NPY following pretreatment with UcnI. Direct PVN injections of NPY (50 pmol) and ghrelin (50 pmol) were orexigenic while UcnI (10-40 pmol) reliably suppressed food intake. Both ghrelin and NPY increased RQ, indicating enhanced utilization of carbohydrates and the preservation of fat stores. UcnI alone suppressed RQ responses. PVN UcnI attenuated the effects of both ghrelin and NPY on food intake and energy substrate utilization. While ghrelin (5 pmol) potentiated the effect of NPY (25 pmol) on RQ and food intake, these responses were inhibited by pretreatment with UcnI (10 pmol). In conclusion, PVN NPY and ghrelin stimulate eating and promote carbohydrate oxidation while inhibiting fat utilization. These effects are blocked by UcnI which alone suppresses appetite and promotes fat oxidation. Overall these findings are consistent with a possible interactive role of PVN NPY, ghrelin and urocortin in the modulation of appetite and energy metabolism.

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Section: Discussionmentioning

confidence: 99%

Urocortin I inhibits the effects of ghrelin and neuropeptide Y on feeding and energy substrate utilization

et al. 2011

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“…The endogenous ligand to this receptor was identified by Kojima et al (1999) as ghrelin (GRLN), which is a 28-amino acid peptide synthesized mainly in the oxyntic mucosal cells of the stomach and which has diverse actions such as potent GH-releasing and orexigenic activities, insulonistasis, cardiovascular effects, stimulation of gastric motility and acid secretion, adipogenesis, and cell proliferation (Muccioli et al 2007, Veldhuis & Bowers 2010.…”

Section: Introductionmentioning

confidence: 99%

A novel GH secretagogue, A233, exhibits enhanced growth activity and innate immune system stimulation in teleosts fish

Martı́nez

Ubieta

Herrera

et al. 2012

Journal of Endocrinology

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In teleosts fish, secretion of GH is regulated by several hypothalamic factors that are influenced by the physiological state of the animal. There is an interaction between immune and endocrine systems through hormones and cytokines. GH in fish is involved in many physiological processes that are not overtly growth related, such as saltwater osmoregulation, antifreeze synthesis, and the regulation of sexual maturation and immune functions. This study was conducted to characterize a decapeptide compound A233 (GKFDLSPEHQ) designed by molecular modeling to evaluate its function as a GH secretagogue (GHS). In pituitary cell culture, the peptide A233 induces GH secretion and it is also able to increase superoxide production in tilapia head-kidney leukocyte cultures. This effect is blocked by preincubation with the GHS receptor antagonist [D-Lys 3 ]-GHRP6. Immunoneutralization of GH by addition of anti-tilapia GH monoclonal antibody blocked the stimulatory effect of A233 on superoxide production. These experiments propose a GH-mediated mechanism for the action of A233. The in vivo biological action of the decapeptide was also demonstrated for growth stimulation in goldfish and tilapia larvae (P!0 . 001). Superoxide dismutase levels, antiprotease activity, and lectin titer were enhanced in tilapia larvae treated with this novel molecule. The decapeptide A233 designed by molecular modeling is able to function as a GHS in teleosts and enhance parameters of the innate immune system in the fish larvae.

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“…Ghrelin has been shown to exhibit orexigenic, prokinetic, insulinostatic, adipogenic, vasodilatory, and immunomodulatory properties (9,10). Ghrelin-producing (X/A-like) cells have been located throughout the intestinal tract in rodents, while the stomach is the richest for these cells (11).…”

Section: Introductionmentioning

confidence: 99%

Prokinetics stimulate the increase of ghrelin in mice

Sagkan-Ozturk¹,

Demir²,

Öztürk³

2017

BLL

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OBJECTIVES: Intestinal motility is regulated by several neurotransmitters and neuropeptides including dopamine and acetylcholine as well as ghrelin. Metoclopramide and domperidone are long-standing treatment options for dysmotility, and erythromycin is suggested in selected patients. In the present study, we aimed to investigate the effects of mentioned prokinetics on ghrelin levels. METHODS: Serum ghrelin levels were estimated by using enzyme-linked immunoassay following a single administration of domperidone, metoclopramide, or erythromycin. RESULTS: Our results showed that both antidopaminergic and cholinergic prokinetics increase the circulating ghrelin levels. There was no signifi cant difference between enteral and parenteral control groups. Also, statistical analysis revealed that neither prokinetic was superior to the other in regard to its ghrelin stimulating effect. CONCLUSION: Conclusively, the present study demonstrated that the circulating levels of ghrelin increase by the administration of antidopaminergic and cholinergic prokinetics. Hence, this effect on ghrelin may partly be responsible for the motility-stimulating actions of domperidone, metoclopramide, and erythromycin (Fig. 2, Ref. 39). Text in PDF www.elis.sk.

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Integrating GHS into the Ghrelin System

Cited by 49 publications

References 640 publications

Urocortin I inhibits the effects of ghrelin and neuropeptide Y on feeding and energy substrate utilization

Urocortin I inhibits the effects of ghrelin and neuropeptide Y on feeding and energy substrate utilization

A novel GH secretagogue, A233, exhibits enhanced growth activity and innate immune system stimulation in teleosts fish

Prokinetics stimulate the increase of ghrelin in mice

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