Ghrelin is Released from Rat Hypothalamic Explants and Stimulates Corticotrophin-releasing Hormone and Arginine-vasopressin

Am, Mozid; Tringali, Giuseppe; Ml, Forsling; Ms, Hendricks; Ajodha, Sharon; Edwards, Robert G.; Navarra, Pierluigi; Grossman, A.; Korbonits, Márta

doi:10.1055/s-2003-41801

Cited by 108 publications

(26 citation statements)

References 17 publications

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“…This is consistent with observations that ghrelin affects synaptogenesis and development of neuronal circuits, as well as modulation of memory processes, sleep patterns and behavior [44,45,46,47,48,49,94,95,96]. Within the hypothalamus-pituitary axis, GHS-R1a mediates ghrelin/GHS modulation of GH, PRL, CRH/ACTH and GnRH/gonadotropin secretion [26,27,28,97,98,99,100,101,102]. Orexigenic effects of ghrelin/GHS are likely mediated by GHS-R1a expressed by hypothalamic neurons containing neuropeptide Y (NPY)/Agouti-related protein [34,103,104,105,106].…”

Section: Type 1a Ghs Receptorsupporting

confidence: 90%

“…Ghrelin was shortly identified as a motilin homologue or the ‘motilin-related polypeptide’ [22, 23], which had been found capable of stimulating gut motility [24, 25]. Since this time, numerous other neuroendocrine effects have been attributed to ghrelin, such as stimulation of CRH, ACTH, PRL secretion and inhibition of GnRH and gonadotropin release [26,27,28]. In addition, non-endocrine and metabolic activities of ghrelin have also been described, notably stimulation of food intake and gut motility [27,29,30,31,32,33], influences on body weight and energy balance [34], insulin release, glucose and lipid metabolism [35,36,37,38,39,40,41,42,43], sleep [44, 45], behavioral responses to stress [46,47,48], learning and memory [49], improvements of cardiovascular performances [50,51,52,53,54], effects on cell proliferation, differentiation, survival and fetal development [55,56,57,58,59,60,61], besides influencing immunological responses [[62], see also for reviews [63,64,65,66]].…”

Section: Introductionmentioning

confidence: 99%

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Heterogeneity of Ghrelin/Growth Hormone Secretagogue Receptors

Muccioli¹,

Baragli²,

Granata³

et al. 2007

Neuroendocrinology

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Ghrelin is a gastric polypeptide displaying strong GH-releasing activity by activation of the type 1a GH secretagogue receptor (GHS-R1a) located in the hypothalamus-pituitary axis. GHS-R1a is a G-protein-coupled receptor that, upon the binding of ghrelin or synthetic peptidyl and non-peptidyl ghrelin-mimetic agents known as GHS, preferentially couples to G_q, ultimately leading to increased intracellular calcium content. Beside the potent GH-releasing action, ghrelin and GHS influence food intake, gut motility, sleep, memory and behavior, glucose and lipid metabolism, cardiovascular performances, cell proliferation, immunological responses and reproduction. A growing body of evidence suggests that the cloned GHS-R1a alone cannot be the responsible for all these effects. The cloned GHS-R1b splice variant is apparently non-ghrelin/GHS-responsive, despite demonstration of expression in neoplastic tissues responsive to ghrelin not expressing GHS-R1a; GHS-R1a homologues sensitive to ghrelin are capable of interaction with GHS-R1b, forming heterodimeric species. Furthermore, GHS-R1a-deficient mice do not show evident abnormalities in growth and diet-induced obesity, suggesting the involvement of another receptor. Additional evidence of the existence of another receptor is that ghrelin and GHS do not always share the same biological activities and activate a variety of intracellular signalling systems besides G_q. The biological actions on the heart, adipose tissue, pancreas, cancer cells and brain shared by ghrelin and the non-acylated form of ghrelin (des-octanoyl ghrelin), which does not bind GHS-R1a, represent the best evidence for the existence of a still unknown, functionally active binding site for this family of molecules. Finally, located in the heart and blood vessels is the scavenger receptor CD36, involved in the endocytosis of the pro-atherogenic oxidized low-density lipoproteins, which is a pharmacologically and structurally distinct receptor for peptidyl GHS and not for ghrelin. This review highlights the most recently discovered features of GHS-R1a and the emerging evidence for a novel group of receptors that are not of the GHS1a type; these appear involved in the transduction of the multiple levels of information provided by GHS and ghrelin.

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Section: Type 1a Ghs Receptorsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Heterogeneity of Ghrelin/Growth Hormone Secretagogue Receptors

Muccioli¹,

Baragli²,

Granata³

et al. 2007

Neuroendocrinology

View full text Add to dashboard Cite

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“…Ghrelin stimulates the HPA axis in the rat directly and by stimulation of both CRH, and arginine vassopresin (AVP) release from the hypothalamus (Mozid et al 2003). At the pituitary level, we have demonstrated (Stevanović et al 2006), in agreement with others (Wren et al 2000;Arvat et al 2001), that centrally administered ghrelin stimulated both pituitary adrenocorticotrophic hormone (ACTH) and corticosterone secretion.…”

Section: Introductionsupporting

confidence: 89%

Central effects of ghrelin on the adrenal cortex: a morphological and hormonal study

VLj¹,

Dm²,

Dm³

et al. 2010

gpb

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Abstract. Ghrelin, a growth hormone secretagogue that exerts an important role in appetite and weight regulation, participates in the activation of the hypothalamo-pituitary-adrenal (HPA) axis. Male Wistar rats (5/group) received daily for 5 days, via an ICV (intracerebroventricular) cannula, 5 µl phosphate buffered saline with or without 1 µg of rat ghrelin. Two hours after the last injection, blood and adrenal glands were collected from decapitated rats for blood hormone analyses and histologic and morphometric processing. Ghrelin treatment resulted in increased (p < 0.05) body weight (13%), absolute whole adrenal gland weight (18%) and whole adrenal gland volume (20%). The absolute volumes of the entire adrenal cortex, ZG, ZF, and ZR also increased (p < 0.05) after ghrelin by 20%, 21%, 21% and 11%, respectively. Ghrelin-treated rats had elevated (p < 0.05) blood concentrations of ACTH, aldosterone and corticosterone (68%, 32% and 67%, respectively). The data clearly provide both morphological and hormonal status that ghrelin acts centrally to exert a global stimulatory effect on the adrenal cortex. Clarifying of the ghrelin precise role in the multiple networks affecting the stress hormone release, besides its well known energy and metabolic disbalance effects, remains a very important research goal.

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“…Furthermore, repeated [50,51,52] but inconsistent [53] findings indicate that ghrelin, being not only a link between the nervous and endocrine systems but also part of a circuit relevant in depression [54] and crucially involved in sleep regulation [55], increases noradrenergic transmission in the hypothalamus, supporting an antidepressant action; decreased central monoaminergic function is an established hypothesis for the etiopathogenesis of depression [54]. In contrast, ghrelin’s suppressive effect on central release of another monoamine, namely serotonin [53], suggests a depressogenic effect, such as its stimulatory action on the hypothalamic-pituitary-adrenal axis [56,57,58,59]; hyperactivity of the hypothalamic-pituitary-adrenal axis is another model for the development of depression [59]. We also reported that an antidepressant-like effect of antisense DNA for ghrelin in rats suggests a depressogenic effect [42].…”

Section: Discussionmentioning

confidence: 99%

Serum Ghrelin Levels and the Effects of Antidepressants in Major Depressive Disorder and Panic Disorder

Ishitobi

Kohno²,

Kanehisa³

et al. 2012

Neuropsychobiology

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Background: Two opposing models for the action of ghrelin in the behavioral responses to stress were recently proposed. Some studies suggest that an increase in ghrelin contributes to the mechanisms responsible for the development of stress-induced depression and anxiety, while others suggest that it helps minimize what otherwise would be more severe manifestations of depression and anxiety following stress. Methods: We measured serum ghrelin levels, Profile of Mood States (POMS) scores and State-Trait Anxiety Inventory scores in nonresponders (treatment-resistant patients; 30) and responders (38) with major depressive disorder (MDD), nonresponders (29) and responders (51) with panic disorder and 97 healthy controls. Results: The ghrelin concentration in nonresponders with MDD was higher than that of responders with MDD and normal controls. The ghrelin concentration in nonresponders with panic disorder was higher than that of normal controls. POMS vigor scores in patients with MDD and panic disorder were significantly decreased compared with those in healthy controls. Other POMS scores in patients with MDD and panic disorder were significantly increased compared with those of healthy controls. Trait and state anxiety of the State-Trait Anxiety Inventory in MDD and panic disorder patients were higher than those in healthy controls. Conclusions: These results indicate that decreased serum ghrelin levels might be associated with antidepressant treatment to confer the maximum therapeutic effect in patients with MDD and panic disorder.

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Ghrelin is Released from Rat Hypothalamic Explants and Stimulates Corticotrophin-releasing Hormone and Arginine-vasopressin

Cited by 108 publications

References 17 publications

Heterogeneity of Ghrelin/Growth Hormone Secretagogue Receptors

Heterogeneity of Ghrelin/Growth Hormone Secretagogue Receptors

Central effects of ghrelin on the adrenal cortex: a morphological and hormonal study

Serum Ghrelin Levels and the Effects of Antidepressants in Major Depressive Disorder and Panic Disorder

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