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Transcriptional Dynamics During Human Adipogenesis and Its Link to Adipose Morphology and Distribution
Karolinska Inst, Dept Med, Stockholm, Sweden.
Karolinska Inst, Dept Med, Stockholm, Sweden.
Karolinska Inst, Dept Med, Stockholm, Sweden.
Univ Copenhagen, Dept Biol, Bioinformat Ctr, Copenhagen, Denmark;Univ Copenhagen, Biotech Res & Innovat Ctr, Copenhagen, Denmark.ORCID-id: 0000-0003-1516-879X
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2017 (Engelska)Ingår i: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 66, nr 1, s. 218-230Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

White adipose tissue (WAT) can develop into several phenotypes with different pathophysiological impact on type 2 diabetes. To better understand the adipogenic process, the transcriptional events that occur during in vitro differentiation of human adipocytes were investigated and the findings linked to WAT phenotypes. Single molecule transcriptional profiling provided a detailed map of the expressional changes of genes, enhancers, and long noncoding RNAs, where different types of transcripts share common dynamics during differentiation. Common signatures include early downregulated, transient, and late induced transcripts, all of which are linked to distinct developmental processes during adipogenesis. Enhancers expressed during adipogenesis overlap significantly with genetic variants associated with WAT distribution. Transiently expressed and late induced genes are associated with hypertrophic WAT (few but large fat cells), a phenotype closely linked to insulin resistance and type 2 diabetes. Transcription factors that are expressed early or transiently affect differentiation and adipocyte function and are controlled by several well-known upstream regulators such as glucocorticosteroids, insulin, cAMP, and thyroid hormones. Taken together, our results suggest a complex but highly coordinated regulation of adipogenesis.

Ort, förlag, år, upplaga, sidor
2017. Vol. 66, nr 1, s. 218-230
Nationell ämneskategori
Endokrinologi och diabetes
Identifikatorer
URN: urn:nbn:se:uu:diva-361227DOI: 10.2337/db16-0631ISI: 000390834300025PubMedID: 27803022OAI: oai:DiVA.org:uu-361227DiVA, id: diva2:1250885
Forskningsfinansiär
VetenskapsrådetNovo Nordisk, NNF14OC0010187 NNF10SA1016550 NNF15OC0015894Tillgänglig från: 2018-09-25 Skapad: 2018-09-25 Senast uppdaterad: 2018-09-25Bibliografiskt granskad

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Ingelsson, Erik

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Andersson, RobinItoh, MasayoshiLassmann, TimoCarninci, PieroForrest, Alistair R. R.Sandelin, AlbinIngelsson, Erik
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Science for Life Laboratory, SciLifeLabMolekylär epidemiologi
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Diabetes
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