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Prolactin-releasing peptide improved leptin hypothalamic signaling in obese mice
M. Holubová, L. Hrubá, B. Neprašová, Z. Majerčíková, Z. Lacinová, J. Kuneš, L. Maletínská, B. Železná,
Language English Country England, Great Britain
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 1997 to 12 months ago
Freely Accessible Science Journals
from 1997 to 12 months ago
Open Access Digital Library
from 1988-07-01
Open Access Digital Library
from 1997-09-01
PubMed
29233862
DOI
10.1530/jme-17-0171
Knihovny.cz E-resources
- MeSH
- Apoptosis MeSH
- Phosphorylation MeSH
- Prolactin-Releasing Hormone metabolism MeSH
- Hypothalamus metabolism MeSH
- Leptin metabolism MeSH
- Receptors, Leptin metabolism MeSH
- Humans MeSH
- RNA, Messenger genetics metabolism MeSH
- Mice, Inbred C57BL MeSH
- Mice, Obese MeSH
- Neurons metabolism MeSH
- Fasting blood MeSH
- Eating MeSH
- Signal Transduction * MeSH
- Organ Size MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't 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.
References provided by Crossref.org
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