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Lipocalin 13 enhances insulin secretion but is dispensable for systemic metabolic control.

Life Sci. All. 4:e202000898 (2021)
Verlagsversion DOI
Open Access Gold
Creative Commons Lizenzvertrag
Members of the lipocalin protein family serve as biomarkers for kidney disease and acute phase inflammatory reactions, and are under preclinical development for the diagnosis and therapy of allergies. However, none of the lipocalin family members has made the step into clinical development, mostly due to their complex biological activity and the lack of in-depth mechanistic knowledge. Here, we show that the hepatokine lipocalin 13 (LCN13) triggers glucose-dependent insulin secretion and cell proliferation of primary mouse islets. However, inhibition of endogenous LCN13 expression in lean mice did not alter glucose and lipid homeostasis. Enhanced hepatic secretion of LCN13 in either diet-induced or genetic obesity led to no discernible impact on systemic glucose and lipid metabolism, neither in preventive nor therapeutic setting. Of note, loss or forced LCN13 hepatic secretion did not trigger any compensatory regulation of related lipocalin family members. Together, these data are in stark contrast to the suggested gluco-regulatory and therapeutic role of LCN13 in obesity, and imply complex regulatory steps in LCN13 biology at the organismic level mitigating its principal insulinotropic effects.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Adenoassociated Virus Serotype-8; Immune-responses; Fetuin-a; Alpha(1)-acid Glycoprotein; Gut Microbiota; In-vivo; Resistance; Expression; Adenovirus; Receptor
ISSN (print) / ISBN 2575-1077
e-ISSN 2575-1077
Zeitschrift Life Science Alliance
Quellenangaben Band: 4, Heft: 4, Seiten: , Artikelnummer: e202000898 Supplement: ,
Verlag EMBO Press
Verlagsort Heidelberg
Begutachtungsstatus Peer reviewed
Förderungen Collaborative Research Center 1118 "Reactive metabolites and diabetic complications"