Obesity develops early in childhood and is accompanied by early signs of adipose tissue
(AT) dysfunction and metabolic disease in children. In order to analyse the molecular processes during
obesity-related AT accumulation in children, we investigated genome-wide expression profiles in AT
samples, isolated adipocytes, and stromal vascular fraction (SVF) cells and assessed their relation to
obesity as well as biological and functional AT parameters. We detected alterations in gene expression
associated with obesity and related parameters, i.e., BMI SDS, adipocyte size, macrophage infiltration,
adiponectin, and/or leptin. While differential gene expression in AT and adipocytes shared an
enrichment in metabolic pathways and pathways related to extracellular structural organisation, SVF
cells showed an overrepresentation in inflammatory pathways. In adipocytes, we found the strongest
positive association for epidermal growth factor-like protein 6 (EGFL6) with adipocyte hypertrophy.
EGFL6 was also upregulated during in vitro adipocyte differentiation. In children, EGFL6 expression
was positively correlated to parameters of AT dysfunction and metabolic disease such as macrophage
infiltration into AT, hs-CRP, leptin levels, and HOMA-IR. In conclusion, we provide evidence for
early alterations in AT gene expression related to AT dysfunction in children and identified EGFL6 as
potentially being involved in processes underlying the pathogenesis of metabolic disease.
| Identifer | oai:union.ndltd.org:DRESDEN/oai:qucosa:de:qucosa:89052 |
| Date | 16 January 2024 |
| Creators | Landgraf, Kathrin, Kühnapfel, Andreas, Schlanstein, Maria, Biemann, Ronald, Isermann, Berend, Kempf, Elena, Kirsten, Holger, Scholz, Markus, Körner, Antje |
| Publisher | MDPI |
| Source Sets | Hochschulschriftenserver (HSSS) der SLUB Dresden |
| Language | English |
| Detected Language | English |
| Type | info:eu-repo/semantics/publishedVersion, doc-type:article, info:eu-repo/semantics/article, doc-type:Text |
| Rights | info:eu-repo/semantics/openAccess |
| Relation | 4349 |
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