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Sabikunnahar, B.* ; Caldwell, S.* ; Varnum, S.* ; Hogan, T.* ; Lahue, K.G.* ; Rathkolb, B. ; Gerlini, R. ; Dragano, N.R.V. ; Aguilar-Pimentel, J.A. ; Irmler, M. ; Sanz-Moreno, A. ; da Silva Buttkus, P. ; Beckers, J. ; Wolf, E.* ; Gailus-Durner, V. ; Fuchs, H. ; Hrabě de Angelis, M. ; Ather, J.L.* ; Poynter, M.E.* ; Krementsov, D.N.*

LncRNA U90926 is dispensable for the development of obesity-associated phenotypes in vivo.

Physiol. Rep. 12:e15901 (2024)
Verlagsversion DOI PMC
Creative Commons Lizenzvertrag
Obesity is a global health problem characterized by excessive fat accumulation, driven by adipogenesis and lipid accumulation. Long non-coding RNAs (lncRNAs) have recently been implicated in regulating adipogenesis and adipose tissue function. Mouse lncRNA U90926 was previously identified as a repressor of in vitro adipogenesis in 3T3-L1 preadipocytes. Consequently, we hypothesized that, in vivo, U90926 may repress adipogenesis, and hence its deletion would increase weight gain and adiposity. We tested the hypothesis by applying U90926-deficient (U9-KO) mice to a high-throughput phenotyping pipeline. Compared with WT, U9-KO mice showed no major differences across a wide range of behavioral, neurological, and other physiological parameters. In mice fed a standard diet, we have found no differences in obesity-related phenotypes, including weight gain, fat mass, and plasma concentrations of glucose, insulin, triglycerides, and free fatty acids, in U9-KO mice compared to WT. U90926 deficiency lacked a major effect on white adipose tissue morphology and gene expression profile. Furthermore, in mice fed a high-fat diet, we found increased expression of U90926 in adipose tissue stromal vascular cell fraction, yet observed no effect of U90926 deficiency on weight gain, fat mass, adipogenesis marker expression, and immune cell infiltration into the adipose tissue. These data suggest that the U90926 lacks an essential role in obesity-related phenotypes and adipose tissue biology in vivo.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Lncrna ; U90926 ; Adipogenesis ; Obesity; Long Noncoding Rnas; Adipose-tissue; Gene-expression; Adipogenesis; Adipocyte; Cellularity; Cell; Differentiation; Inflammation; Growth
ISSN (print) / ISBN 2051-817X
e-ISSN 2051-817X
Zeitschrift Physiological reports
Quellenangaben Band: 12, Heft: 1, Seiten: , Artikelnummer: e15901 Supplement: ,
Verlag Wiley
Verlagsort 111 River St, Hoboken 07030-5774, Nj Usa
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Experimental Genetics (IEG)
Förderungen HHS | NIH | NIAID | Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases (DMID)