Ghrelin is an orexigenic and metabolic signaling peptide in the arcuate and paraventricular nuclei

Currie, Paul J.; Mirza, Aaisha; Fuld, Rebecca; Park, Diana; Vasselli, Joseph R.

doi:10.1152/ajpregu.00756.2004

Cited by 111 publications

(104 citation statements)

References 70 publications

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“…A microinjection of ghrelin into the PVN or ARC increases food intake and RQ in rats (Currie et al 2005). Since the PVN and ARC express GHS-R1a (Zigman et al 2006), these findings together with our present results may indicate that ghrelin directly activates GHS-R1a in the PVN and ARC and induces a suppressive effect on the sympathetic nervous system innervating BAT.…”

Section: Discussionsupporting

confidence: 79%

“…5-10 nmol for i.v. administration (Nakazato et al 2001, Date et al 2002, Currie et al 2005. We also administered rat des-acyl ghrelin (Peptide Institute, Inc.), which does not bind to GHS-R1a, at a dose of 500 pmol for i.c.v.…”

Section: Microdialysis Of Noradrenaline In Batmentioning

confidence: 99%

“…or peripherally also increases the respiratory quotient (RQ), indicating its inhibitory action on fat expenditure (Tschöp et al 2000). Furthermore, the microinjection of ghrelin into the PVN or ARC increases food intake and RQ (Currie et al 2005). Therefore, the central effect of ghrelin on energy homeostasis may be mediated through the activation of GHS-R1a in the PVN and ARC.…”

Section: Introductionmentioning

confidence: 99%

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Ghrelin suppresses noradrenaline release in the brown adipose tissue of rats

Mano-Otagiri¹,

Ohata²,

Iwasaki-Sekino³

et al. 2009

Journal of Endocrinology

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To clarify the role of ghrelin in the regulatory mechanism of energy metabolism, we analyzed the effects of centrally and peripherally administered ghrelin on noradrenaline release in the brown adipose tissue (BAT) of rats using a microdialysis system. I.c.v. administration of ghrelin at a dose of 500 pmol suppressed noradrenaline release in BAT, and microinjection of ghrelin (50 pmol) into the paraventricular nucleus (PVN) or arcuate nucleus (ARC) of the hypothalamus also suppressed noradrenaline release in BAT. In addition, i.v. administered ghrelin (30 nmol) suppressed noradrenaline release in BAT, and this suppression was blocked by a vagotomy. Neither i.c.v. nor i.v. administration of des-acyl ghrelin, which does not bind to GH secretagogue receptor type 1a (GHS-R1a), affected noradrenaline release in BAT. These results indicate that ghrelin increases energy storage by suppressing the activity of the sympathetic nerve innervating BAT. It seems that the PVN and ARC, which express GHSR1a, are the sites of action of ghrelin in the brain and that the action of peripheral ghrelin on the sympathetic nerve activity innervating BAT is mediated by the vagal nerve, which also expresses GHS-R1a.

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Section: Discussionsupporting

confidence: 79%

Section: Microdialysis Of Noradrenaline In Batmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Ghrelin suppresses noradrenaline release in the brown adipose tissue of rats

Mano-Otagiri¹,

Ohata²,

Iwasaki-Sekino³

et al. 2009

Journal of Endocrinology

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“…Circulating ghrelin levels as well as gastric ghrelin mRNA expression have been reported to increase after fasting and decrease rapidly after refeeding (Tschop et al, 2000). Ghrelin stimulates eating when injected into the arcuate and paraventricular nuclei (Currie et al, 2005), and we have shown here that ghrelin resets the SCN clock when applied directly to SCN tissue during the subjective day. Moreover, gastric ghrelin has been found to affect gastric per1 and per2 expression, suggesting that it can also be considered as a signal regulating peripheral oscillators .…”

Section: Discussionsupporting

confidence: 55%

“…Besides the SCN, the arcuate nuclei (Mistlberger and Antle, 1999), the paraventricular nuclei (Kalra et al, 1999;Currie et al, 2005), the dorsomedial hypothalamus (Gooley et al, 2006;Landry et al, 2006), and the digestive system (Davidson et al, 2003) have also been suggested to be important for food entrainment.…”

Section: Introductionmentioning

confidence: 99%

Ghrelin Effects on the Circadian System of Mice

Yannielli

Molyneux²,

Harrington³

et al. 2007

J. Neurosci.

122

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The orexigenic peptide ghrelin stimulates both food intake and growth hormone release and is synthesized in the stomach and in hypothalamic areas involved in feeding control. The suprachiasmatic nuclei of the hypothalamus (SCN) control most circadian rhythms, although there is evidence that some oscillators, such as food-entrainable oscillators, can drive activity rhythms even after SCN ablation. Ghrelin levels exhibit a circadian rhythm and closely follow feeding schedules, making this peptide a putative candidate for food-related entraining signals. We examined the response of the SCN to ghrelin treatments in vitro, by means of electrophysiological and bioluminescence recordings, and in vivo, by assessing effects on the phase of locomotor activity rhythms. Ghrelin applied at circadian time 6 in vitro to cultured SCN slices induced an ϳ3 h phase advance. In addition, ghrelin phase advanced the rhythm of PER2::LUC (Period2::Luciferase) expression in cultured SCN explants from mPer2Luc transgenic mice. In vivo, intraperitoneal administration of ghrelin or a synthetic analog, growth hormone-releasing protein-6 (GHRP-6), to ad libitum fed animals failed to alter circadian phase. When injected after 30 h of food deprivation, GHRP-6 induced a phase advance compared with saline-injected animals. These results indicate that ghrelin may play a role in the circadian system by exerting a direct action on the SCN and that the system as a whole may become sensitive to ghrelin and other feeding-related neuropeptides under conditions of food restriction.

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Elevated ghrelin alters the behavioral effects of perinatal acetaminophen exposure in rats

Herrington

Darwich

Harshaw

et al. 2022

Developmental Psychobiology

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A growing body of evidence links prenatal and early postnatal acetaminophen (APAP) exposure to atypical development of brain and behavior. In adult rodents, APAP is known to produce oxidative stress and lower anxiety-related behavior following acute exposure. In models of early-life exposure, APAP has also been shown to alter anxietyrelated and other behaviors. Since the neuropeptide ghrelin has been recently shown to reduce oxidative stress markers and act as a neuroprotectant, we hypothesized that exposure to ghrelin prior to exposure to APAP would mitigate the behavioral effects of APAP exposure. On postnatal day 7, pups were administered doses of either APAP (51.97 mg/kg), ghrelin (1 mg/kg/ml), ghrelin + APAP, or vehicle only. As adults, anxietyrelated behavior was assessed in the open field and elevated plus maze. Behavior differed based upon treatment condition. In rats unexposed to ghrelin, APAP treatment resulted in increased exploration (i.e., reduced anxiety) in the open field relative to controls. Rats co-administered APAP and ghrelin did not differ from vehicle-only controls.No significant effects of APAP or interactions between APAP and ghrelin exposures were observed in the elevated plus maze. These results are the first to demonstrate that ghrelin can mitigate the effects of perinatal APAP exposure in rats.

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Ghrelin is an orexigenic and metabolic signaling peptide in the arcuate and paraventricular nuclei

Cited by 111 publications

References 70 publications

Ghrelin suppresses noradrenaline release in the brown adipose tissue of rats

Ghrelin suppresses noradrenaline release in the brown adipose tissue of rats

Ghrelin Effects on the Circadian System of Mice

Elevated ghrelin alters the behavioral effects of perinatal acetaminophen exposure in rats

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