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Simultaneous treatment with palm-LEAP2(1–14) and feeding high-fat diet attenuates liver lipid metabolism but not obesity: Sign of selective resistance to palm-LEAP2(1–14)
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SYSNO ASEP 0616478 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Simultaneous treatment with palm-LEAP2(1–14) and feeding high-fat diet attenuates liver lipid metabolism but not obesity: Sign of selective resistance to palm-LEAP2(1–14) Tvůrce(i) Peteláková, M. (CZ)
Neprašová, B. (CZ)
Šmotková, Zuzana (FGU-C) ORCID, RID
Myšková, A. (CZ)
Holá, L. (CZ)
Petelák, A. (CZ)
Áčová, A. (CZ)
Cantel, S. (FR)
Fehrentz, J. A. (FR)
Sýkora, D. (CZ)
Kuneš, Jaroslav (FGU-C) RID, ORCID
Železná, B. (CZ)
Maletínská, L. (CZ)Číslo článku 112442 Zdroj.dok. Molecular and Cellular Endocrinology. - : Elsevier - ISSN 0303-7207
Roč. 597, February (2025)Poč.str. 14 s. Jazyk dok. eng - angličtina Země vyd. NL - Nizozemsko Klíč. slova palm-LEAP2(1–14) ; LEAP2 ; ghrelin ; diet-induced obesity ; lipid metabolism ; LEAP2 resistance Obor OECD Endocrinology and metabolism (including diabetes, hormones) Způsob publikování Omezený přístup Institucionální podpora FGU-C - RVO:67985823 UT WOS 001394331700001 EID SCOPUS 85212657866 DOI https://doi.org/10.1016/j.mce.2024.112442 Anotace Liver-enriched antimicrobial peptide 2 (LEAP2) is a natural antagonist/inverse agonist of ghrelin receptor GHSR. Its truncated palmitoylated analog palm-LEAP2(1–14) promised anti-obesity properties because it exhibited favourable stability and an acute anorexigenic effect in our previous studies.Here we demonstrate desirable palm-LEAP2(1–14) pharmacokinetics, with significant levels of the peptide persisting in mouse blood 3 h after its subcutaneous administration. Palm-LEAP2 (1–14) reduced ghrelin-induced c-Fos immunoreactivity in arcuate nucleus and area postrema, in line with previously described silencing of ghrelin orexigenic effect. In spite of this, anti-obesity effect was not reached by two-week palm-LEAP2(1–14) treatment in mice with diet-induced obesity. Similarly, palm-LEAP2(1–14) administered simultaneously with high-fat diet feeding for 8 weeks did not protect mice from development of obesity and related biochemical changes. However, palm-LEAP2(1–14) kept its ability to attenuate liver de novo lipogenesis, and prominently lowered liver gene expression of nuclear receptors PPARG, SREBF1 and PPARA, and also expression of lipogenic and lipolytic enzymes.In our recent study, we described a high-fat diet-induced ghrelin resistance, reversible by switch to standard diet, followed by resistance to the acute anorexigenic effects of palm-LEAP2(1–14). Here we conclude that this resistance to palm-LEAP2(1–14) in obesity is probably selective and does not concern its ability to inhibit liver lipid metabolism. Pracoviště Fyziologický ústav Kontakt Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Rok sběru 2026 Elektronická adresa https://doi.org/10.1016/j.mce.2024.112442
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