Prolactin-releasing peptide improved leptin hypothalamic signaling in obese mice
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
29233862
DOI
10.1530/jme-17-0171
PII: JME-17-0171
Knihovny.cz E-zdroje
- Klíčová slova
- FOSB, apoptotic activation, diet-induced obese mice, leptin signaling, prolactin-releasing peptide,
- MeSH
- apoptóza MeSH
- fosforylace MeSH
- hormon uvolňující prolaktin metabolismus MeSH
- hypothalamus metabolismus MeSH
- leptin metabolismus MeSH
- leptinové receptory metabolismus MeSH
- lidé MeSH
- messenger RNA genetika metabolismus MeSH
- myši inbrední C57BL MeSH
- myši obézní MeSH
- neurony metabolismus MeSH
- omezení příjmu potravy krev MeSH
- přijímání potravy MeSH
- signální transdukce * MeSH
- velikost orgánu MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- hormon uvolňující prolaktin MeSH
- leptin MeSH
- leptinové receptory MeSH
- messenger RNA MeSH
The situation following anti-obesity drug termination is rarely investigated, eventhough a decrease in body weight needs to be sustained. Therefore, this study examined the impact of twice-daily peripheral administration of 5 mg/kg [N-palm-γGlu-Lys11] prolactin-releasing peptide 31 (palm11-PrRP31) in mice with diet-induced obesity (DIO from consuming a high-fat diet) after 28 days of treatment (palm11-PrRP31 group) and after 14 days of peptide treatment followed by 14 days of discontinuation (palm11-PrRP31 + saline group). At the end of the treatment, cumulative food intake, body weight and subcutaneous fat weight/body weight ratio and leptin plasma level were reduced significantly in both the palm11-PrRP31 group and the palm11-PrRP31 + saline group compared to the saline control group. This reduction correlated with significantly increased FOSB, a marker of long-term neuronal potentiation, in the nucleus arcuatus and nucleus tractus solitarii, areas known to be affected by the anorexigenic effect of palm11-PrRP31. Moreover, activation of leptin-related hypothalamic signaling was registered through an increase in phosphoinositide-3-kinase, increased phosphorylation of protein kinase B (PKB, AKT) and enhanced extracellular signal-regulated kinase 1/2 phosphorylation. Besides, lowered apoptotic markers c-JUN N-terminal kinase and c-JUN phosphorylation were registered in the hypothalami of both palm11-PrRP31-treated groups. This study demonstrates that palm11-PrRP31 positively affects feeding and leptin-related hypothalamic signaling, not only after 28 days of treatment but even 14 days after the termination of a 14-day long treatment without the yo-yo effect.
Institute for Clinical and Experimental MedicinePrague Czech Republic
Institute of Organic Chemistry and BiochemistryThe Czech Academy of Sciences Czech Republic
Institute of PhysiologyThe Czech Academy of Sciences Prague Czech Republic
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