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Cholecystokinin System Is Involved in the Anorexigenic Effect of Peripherally Applied Palmitoylated Prolactin-Releasing Peptide in Fasted Mice

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F21%3A00545530" target="_blank" >RIV/67985823:_____/21:00545530 - isvavai.cz</a>

  • Nalezeny alternativní kódy

    RIV/61388963:_____/21:00545633 RIV/00216208:11110/21:10432590

  • Výsledek na webu

    <a href="https://www.biomed.cas.cz/physiolres/pdf/2021/70_579.pdf" target="_blank" >https://www.biomed.cas.cz/physiolres/pdf/2021/70_579.pdf</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.33549/physiolres.934694" target="_blank" >10.33549/physiolres.934694</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Cholecystokinin System Is Involved in the Anorexigenic Effect of Peripherally Applied Palmitoylated Prolactin-Releasing Peptide in Fasted Mice

  • Popis výsledku v původním jazyce

    Prolactin-releasing peptide (PrRP) has been proposed to mediate the central satiating effects of cholecystokinin (CCK) through the vagal CCK1 receptor. PrRP acts as an endogenous ligand of G protein-coupled receptor 10 (GPR10), which is expressed at the highest levels in brain areas related to food intake regulation, e.g., the paraventricular hypothalamic nucleus (PVN) and nucleus of the solitary tract (NTS). The NTS and PVN are also significantly activated after peripheral CCK administration. The aim of this study was to determine whether the endogenous PrRP neuronal system in the brain is involved in the central anorexigenic effect of the peripherally administered CCK agonist JMV236 or the CCK1 antagonist devazepide and whether the CCK system is involved in the central anorexigenic effect of the peripherally applied lipidized PrRP analog palm-PrRP31 in fasted lean mice. The effect of devazepide and JMV236 on the anorexigenic effects of palm-PrRP31 as well as devazepide combined with JMV236 and palm-PrRP31 on food intake and Fos cell activation in the PVN and caudal NTS was examined. Our results suggest that the anorexigenic effect of JMV236 is accompanied by activation of PrRP neurons of the NTS in a CCK1 receptor-dependent manner. Moreover, while the anorexigenic effect of palm-PrRP31 was not affected by JMV236, it was partially attenuated by devazepide in fasted mice. The present findings indicate that the exogenously influenced CCK system may be involved in the central anorexigenic effect of peripherally applied palm-PrRP31, which possibly indicates some interaction between the CCK and PrRP neuronal systems.

  • Název v anglickém jazyce

    Cholecystokinin System Is Involved in the Anorexigenic Effect of Peripherally Applied Palmitoylated Prolactin-Releasing Peptide in Fasted Mice

  • Popis výsledku anglicky

    Prolactin-releasing peptide (PrRP) has been proposed to mediate the central satiating effects of cholecystokinin (CCK) through the vagal CCK1 receptor. PrRP acts as an endogenous ligand of G protein-coupled receptor 10 (GPR10), which is expressed at the highest levels in brain areas related to food intake regulation, e.g., the paraventricular hypothalamic nucleus (PVN) and nucleus of the solitary tract (NTS). The NTS and PVN are also significantly activated after peripheral CCK administration. The aim of this study was to determine whether the endogenous PrRP neuronal system in the brain is involved in the central anorexigenic effect of the peripherally administered CCK agonist JMV236 or the CCK1 antagonist devazepide and whether the CCK system is involved in the central anorexigenic effect of the peripherally applied lipidized PrRP analog palm-PrRP31 in fasted lean mice. The effect of devazepide and JMV236 on the anorexigenic effects of palm-PrRP31 as well as devazepide combined with JMV236 and palm-PrRP31 on food intake and Fos cell activation in the PVN and caudal NTS was examined. Our results suggest that the anorexigenic effect of JMV236 is accompanied by activation of PrRP neurons of the NTS in a CCK1 receptor-dependent manner. Moreover, while the anorexigenic effect of palm-PrRP31 was not affected by JMV236, it was partially attenuated by devazepide in fasted mice. The present findings indicate that the exogenously influenced CCK system may be involved in the central anorexigenic effect of peripherally applied palm-PrRP31, which possibly indicates some interaction between the CCK and PrRP neuronal systems.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    30105 - Physiology (including cytology)

Návaznosti výsledku

  • Projekt

    <a href="/cs/project/GA18-10591S" target="_blank" >GA18-10591S: Lipidované analogy peptidu uvolňujícího prolaktin jako potenciální antiobezitika: zkoumání mechanizmu účinku</a><br>

  • Návaznosti

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Ostatní

  • Rok uplatnění

    2021

  • Kód důvěrnosti údajů

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Údaje specifické pro druh výsledku

  • Název periodika

    Physiological Research

  • ISSN

    0862-8408

  • e-ISSN

    1802-9973

  • Svazek periodika

    70

  • Číslo periodika v rámci svazku

    4

  • Stát vydavatele periodika

    CZ - Česká republika

  • Počet stran výsledku

    12

  • Strana od-do

    579-590

  • Kód UT WoS článku

    000693412000009

  • EID výsledku v databázi Scopus

    2-s2.0-85114834528