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