INT144356
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Above all, ghrelin and synthetic GHS possess an acute stimulatory effect on the activity of the hypothalamus-pituitary-adrenal axis in humans, which is, at least, similar to that of the opioid antagonist naloxone, arginine vasopressin and even corticotropin-releasing hormone. | |||||||||||||||
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RESULTS: GHS was present in 52 patients (48.6%) and correlated significantly to shoulder pain at TI, at T2 and at T3 (p < 0.001). | |||||||||||||||
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Long-term surveillance of ghrelin and GHS receptor-deficient and ghrelin-overexpressing transgenic animals will be needed to assess whether prolonged changes in ghrelin availability influence immune function or inflammatory disease.
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Conversely, in a fourth model, transgenic reduction of GHS-R1a expression on GHRH neurons suppressed both GHRH and NPY gene expression, thereby diminishing GH and fat mass in the female [236]. | |||||||||||||||
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Ghrelin, GHS receptors, GH, and GH receptors are expressed in human monocytes and B and T lymphocytes [576]. | |||||||||||||||
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GHS receptors are expressed by both beta and alpha cells [442]. | |||||||||||||||
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Mutational disruption of constitutive GHS-R1a activity is associated with short stature in humans [27], whereas overexpression of GHS-R1a on GHRH neurons augments postweaning growth, reduces fat mass, and augments GHRH and GH gene expression in mice [28]. | |||||||||||||||
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Adult pancreatic islets express relatively little ghrelin protein and few GHS receptors, but fetal and neonatal islets exhibit abundant ghrelin gene transcripts and peptide in epsilon cells [452454]. | |||||||||||||||
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Conversely, overexpression of neuronal GHS-R1a in female mice elevates GH and GHRH gene expression [28]. | |||||||||||||||
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Although physiological effects are not clear, ghrelin is expressed in sheep oocytes [634], and GHS-R1a in Sertoli (nurse) cells in spermatogenic tubules [623]. | |||||||||||||||
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In a third model, overexpression of GHS-R1a in GHRH neurons increased organ and muscle weight, while decreasing body fat in female animals [28]. | |||||||||||||||
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The dorsal motor nucleus of the vagus expresses GHS-R1a, which modulates limbic-system dopamine- and brainstem gaba, glutamine, and noradrenergic transmission to hypothalamic appetitive and satiety centers [335, 341343]. | |||||||||||||||
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Reduced pituitary action of SS is unlikely to be the sole potentiating mechanism subserving GHS action, since GHS and GHRH synergize even after immunoneutralization of SS [268]. | |||||||||||||||
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Although local acylation could explain certain actions of unacylated ghrelin, other effects that oppose or differ from those of acylated peptide raise the possibility of non-GHS-R1a mediation. | |||||||||||||||
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An endogenous ligand for the GHS receptor, acylghrelin, was identified in 1999. | |||||||||||||||
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Thus, GHS-R1a is an amplifier of GHRH outflow as well as a direct effector of pituitary GH secretion. | |||||||||||||||
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Figure 2 depicts a model, which incorporates several major actions of ghrelin/GHS within the GH axis [41]. | |||||||||||||||
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Unlike ghrelin, synthetic GHS's acting via GHS-R1a typically do not require acylation and are not known GOAT substrates. | |||||||||||||||
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In addition, prolonged administration of ghrelin or synthetic GHS in humans augments GH, IGF-I and IGFBP-3 concentrations and lean-body mass, and diminishes total-body fat, while eliciting transient secretion of adenocorticotropin hormone (ACTH), cortisol, and prolactin [64, 269273]. | |||||||||||||||
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The basis may involve pregnancy-associated suppression of hypothalamic GHRH and GHS-R1a with reciprocal induction of the SS gene due to feedback by high placental somatomammotropin (GH isotype V) and maternal IGF-I concentrations [422]. | |||||||||||||||
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