Inhibition of ghrelin-induced feeding in rats by pretreatment with a novel dual orexin receptor antagonist

So, Mariko; Hashimoto, Hirofumi; Saito, Reiko; Yamamoto, Yukiyo; Motojima, Yasuhito; Ueno, Hiroki; Sonoda, Shozo; Yoshimura, Mitsuhiro; Maruyama, Takashi; Kusuhara, Koichi; Ueta, Yoichi

doi:10.1007/s12576-016-0517-5

Cited by 17 publications

(7 citation statements)

References 36 publications

(53 reference statements)

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“…In support of this hypothesis, GHSR is present in the LHA . Intra‐LHA administration of ghrelin increases FOS in the PVN and the administration of orexin receptor antagonists reverses the effects of ICV‐injected ghrelin on c‐FOS expression in the PVN . Interestingly, des‐acyl‐ghrelin also increases c‐FOS expression in PVN neurons after both peripheral and ICV administration, this increase, however, is less than the one achieved by ghrelin administration.…”

Section: The Pvn As a Mediator Of The Action Of Ghrelin On Energy Balmentioning

confidence: 84%

The actions of ghrelin in the paraventricular nucleus: energy balance and neuroendocrine implications

Dos‐Santos

Reis

Perelló³

et al. 2019

Annals of the New York Academy of Sciences

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Ghrelin is a peptide mainly produced and secreted by the stomach. Since its discovery, the impact of ghrelin on the regulation of food intake has been the most studied function of this hormone; however, ghrelin affects a wide range of physiological systems, many of which are controlled by the hypothalamic paraventricular nucleus (PVN). Several pathways may mediate the effects of ghrelin on PVN neurons, such as direct or indirect effects mediated by circumventricular organs and/or the arcuate nucleus. The ghrelin receptor is expressed in PVN neurons, and the peripheral or intracerebroventricular administration of ghrelin affects PVN neuronal activity. Intra-PVN application of ghrelin increases food intake and decreases fat oxidation, which chronically contribute to the increased adiposity. Additionally, ghrelin modulates the neuroendocrine axes controlled by the PVN, increasing the release of vasopressin and oxytocin by magnocellular neurons and corticotropin-releasing hormone by neuroendocrine parvocellular neurons, while possibly inhibiting the release of thyrotropin-releasing hormone. Thus, the PVN is an important target for the actions of ghrelin. Our review discusses the mechanisms of ghrelin actions in the PVN, and its potential implications for energy balance, neuroendocrine, and integrative physiological control.

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Section: The Pvn As a Mediator Of The Action Of Ghrelin On Energy Balmentioning

confidence: 84%

The actions of ghrelin in the paraventricular nucleus: energy balance and neuroendocrine implications

Dos‐Santos

Reis

Perelló³

et al. 2019

Annals of the New York Academy of Sciences

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“…Increasing evidence in clinical studies has revealed that patients with eating disorders, including food consumption, are almost entirely neglected in patients with chronic pain, which may induce a worse prognosis or a more severe pain perception 28 . Central and peripheral administration of ghrelin increases food intake dramatically in rats and mice, which may be due to activation of various brain regions, including the feeding-related areas such as the paraventricular nucleus (PVN) in rats 29,30 . So, we cannot ignore the fact the effects of ghrelin on feeding behaviour and this may alter pain sensitivity throughout the day, which will be worth a very good direction for further study in the future.…”

Section: Discussionmentioning

confidence: 99%

Effects of ghrelin on pGSK-3β and β-catenin expression when protects against neuropathic pain behavior in rats challenged with chronic constriction injury

Peng

Zha

Yang

et al. 2019

Sci Rep

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Ghrelin has been shown to alleviate neuropathic pain by inhibiting the release of proinflammatory cytokines. The purpose of this study was to investigate the role of GSK-3β/β-catenin signaling in mediating the effect of ghrelin on neuropathic pain and to understand the associated mechanisms. Chronic constriction injury (CCI) of the sciatic nerve was used to establish a rat model of neuropathic pain. Hyperalgesia and allodynia were evaluated by observing the mechanical withdrawal threshold and the thermal withdrawal latency. Wnt3a and β-catenin protein expression and GSK-3β phosphorylation were detected by western blotting analysis. The levels of tumor necrosis factor-α and IL-1β were determined using an enzyme-linked immunosorbent assay. In addition, we used immunohistochemical analysis to determine the levels of GSK-3β phosphorylation in the dorsal horn of the spinal cord. Intrathecal delivery of ghrelin effectively ameliorated CCI-induced mechanical allodynia and thermal hyperalgesia at 7 and 14 days and reduced the levels of tumor necrosis factor-α. Ghrelin inhibited CCI-induced GSK-3β activation and β-catenin overexpression in the spinal dorsal horn. Moreover, intrathecal injection of ghrelin suppressed the activation of GSK-3β in the spinal dorsal horn of CCI rats, as assessed by immunohistochemical analysis. Our data indicated that ghrelin could markedly alleviate neuropathic pain by inhibiting the expression of β-catenin, via the suppression of GSK-3β activation, in the spinal cord of CCI rats.

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“…HO axons directly contact NPY and POMC neurons in the arcuate nucleus of rats and signaling through these axons has been shown to regulate their activity in a manner reciprocal to leptin ( Muroya et al, 2004 ). Moreover, ghrelin-induced food intake is significantly reduced in mice pretreated with antibodies against HO and HO knockout mice ( So et al, 2018 ). In the context of sleep deprivation, the activity of HO neurons increases to maintain wakefulness against increased pressure to sleep ( Wu et al, 2002 ).…”

Section: Sleep Disruption-induced Changes To Systemic Physiologymentioning

confidence: 99%

Sleep Disruption and Cancer: Chicken or the Egg?

2022

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Sleep is a nearly ubiquitous phenomenon across the phylogenetic tree, highlighting its essential role in ensuring fitness across evolutionary time. Consequently, chronic disruption of the duration, timing, or structure of sleep can cause widespread problems in multiple physiological systems, including those that regulate energy balance, immune function, and cognitive capacity, among others. Many, if not all these systems, become altered throughout the course of cancer initiation, growth, metastatic spread, treatment, and recurrence. Recent work has demonstrated how changes in sleep influence the development of chronic diseases, including cancer, in both humans and animal models. A common finding is that for some cancers (e.g., breast), chronic disruption of sleep/wake states prior to disease onset is associated with an increased risk for cancer development. Additionally, sleep disruption after cancer initiation is often associated with worse outcomes. Recently, evidence suggesting that cancer itself can affect neuronal circuits controlling sleep and wakefulness has accumulated. Patients with cancer often report difficulty falling asleep, difficulty staying asleep, and severe fatigue, during and even years after treatment. In addition to the psychological stress associated with cancer, cancer itself may alter sleep homeostasis through changes to host physiology and via currently undefined mechanisms. Moreover, cancer treatments (e.g., chemotherapy, radiation, hormonal, and surgical) may further worsen sleep problems through complex biological processes yet to be fully understood. This results in a “chicken or the egg” phenomenon, where it is unclear whether sleep disruption promotes cancer or cancer reciprocally disrupts sleep. This review will discuss existing evidence for both hypotheses and present a framework through which the interactions between sleep and cancer can be dissociated and causally investigated.

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Inhibition of ghrelin-induced feeding in rats by pretreatment with a novel dual orexin receptor antagonist

Cited by 17 publications

References 36 publications

The actions of ghrelin in the paraventricular nucleus: energy balance and neuroendocrine implications

The actions of ghrelin in the paraventricular nucleus: energy balance and neuroendocrine implications

Effects of ghrelin on pGSK-3β and β-catenin expression when protects against neuropathic pain behavior in rats challenged with chronic constriction injury

Sleep Disruption and Cancer: Chicken or the Egg?

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