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Open Access Gold as soon as Publ. Version/Full Text is submitted to ZB.
COBL, MKX and MYOC are potential regulators of brown adipose tissue development associated with obesity-related metabolic dysfunction in children.
Int. J. Mol. Sci. 24:20 (2023)
Obesity is already accompanied by adipose tissue (AT) dysfunction and metabolic disease in children and increases the risk of premature death. Due to its energy-dissipating function, brown AT (BAT) has been discussed as being protective against obesity and related metabolic dysfunction. To analyze the molecular processes associated with BAT development, we investigated genome-wide expression profiles in brown and white subcutaneous and perirenal AT samples of children. We identified 39 upregulated and 26 downregulated genes in uncoupling protein 1 (UCP1)-positive compared to UCP1-negative AT samples. We prioritized for genes that had not been characterized regarding a role in BAT biology before and selected cordon-bleu WH2 repeat protein (COBL), mohawk homeobox (MKX) and myocilin (MYOC) for further functional characterization. The siRNA-mediated knockdown of Cobl and Mkx during brown adipocyte differentiation in vitro resulted in decreased Ucp1 expression, while the inhibition of Myoc led to increased Ucp1 expression. Furthermore, COBL, MKX and MYOC expression in the subcutaneous AT of children is related to obesity and parameters of AT dysfunction and metabolic disease, such as adipocyte size, leptin levels and HOMA-IR. In conclusion, we identify COBL, MKX and MYOC as potential regulators of BAT development and show an association of these genes with early metabolic dysfunction in children.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Cobl ; Mkx ; Myoc ; Adipocyte Differentiation ; Adipose Tissue ; Brown Adipose Tissue ; Children ; Metabolic Disease ; Obesity ; White Adipose Tissue; Transcription Factor Mohawk; Mesenchymal Stem-cells; Cordon-bleu; Thermogenic Adipocytes; Cold-exposure; Ppar-gamma; Gene; White; Differentiation; Identification
ISSN (print) / ISBN
1422-0067
e-ISSN
1661-6596
Quellenangaben
Volume: 24,
Issue: 4,
Article Number: 20
Publisher
MDPI
Publishing Place
Basel
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)