Transcriptional dynamics during human adipogenesis and its link to adipose morphology and distribution
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Transcriptional dynamics during human adipogenesis and its link to adipose morphology and distribution. / Ehrlund, Anna; Mejhert, Niklas; Björk, Christel; Andersson, Robin; Kulyté, Agné; Åström, Gaby; Itoh, Masayoshi; Kawaji, Hideya; Lassmann, Timo; Daub, Carsten O.; Carninci, Piero; Forrest, Alistair R. R.; Hayashizaki, Yoshihide; Sandelin, Albin Gustav; Ingelsson, Erik; FANTOM Consortium; Rydén, Mikael; Laurencikiene, Jurga; Arner, Peter; Arner, Erik.
I: Diabetes, Bind 66, Nr. 1, 2017, s. 218-230.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - Transcriptional dynamics during human adipogenesis and its link to adipose morphology and distribution
AU - Ehrlund, Anna
AU - Mejhert, Niklas
AU - Björk, Christel
AU - Andersson, Robin
AU - Kulyté, Agné
AU - Åström, Gaby
AU - Itoh, Masayoshi
AU - Kawaji, Hideya
AU - Lassmann, Timo
AU - Daub, Carsten O.
AU - Carninci, Piero
AU - Forrest, Alistair R. R.
AU - Hayashizaki, Yoshihide
AU - Sandelin, Albin Gustav
AU - Ingelsson, Erik
AU - FANTOM Consortium, null
AU - Rydén, Mikael
AU - Laurencikiene, Jurga
AU - Arner, Peter
AU - Arner, Erik
N1 - © 2016 by the American Diabetes Association.
PY - 2017
Y1 - 2017
N2 - 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 non-coding RNAs, where different types of transcripts share common dynamics during differentiation. Common signatures include early down-regulated, 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 and late-induced expressed 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, cyclic AMP and thyroid hormones. Taken together, our results suggest a complex, but highly coordinated regulation of adipogenesis.
AB - 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 non-coding RNAs, where different types of transcripts share common dynamics during differentiation. Common signatures include early down-regulated, 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 and late-induced expressed 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, cyclic AMP and thyroid hormones. Taken together, our results suggest a complex, but highly coordinated regulation of adipogenesis.
U2 - 10.2337/db16-0631
DO - 10.2337/db16-0631
M3 - Journal article
C2 - 27803022
VL - 66
SP - 218
EP - 230
JO - Diabetes
JF - Diabetes
SN - 0012-1797
IS - 1
ER -
ID: 169385570