The Adipocyte Acquires a Fibroblast-Like Transcriptional Signature in Response to a High Fat Diet.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
11 02 2020
Historique:
received: 28 10 2019
accepted: 20 01 2020
entrez: 13 2 2020
pubmed: 13 2 2020
medline: 11 11 2020
Statut: epublish

Résumé

Visceral white adipose tissue (vWAT) expands and undergoes extensive remodeling during diet-induced obesity. Much is known about the contribution of various stromal vascular cells to the remodeling process, but less is known of the changes that occur within the adipocyte as it becomes progressively dysfunctional. Here, we performed a transcriptome analysis of isolated vWAT adipocytes to assess global pathway changes occurring in response to a chronic high fat diet (HFD). The data demonstrate that the adipocyte responds to the HFD by adopting a fibroblast-like phenotype, characterized by enhanced expression of ECM, focal adhesion and cytoskeletal genes and suppression of many adipocyte programs most notably those associated with mitochondria. This study reveals that during obesity the adipocyte progressively becomes metabolically dysfunctional due to its acquisition of fibrogenic functions. We propose that mechano-responsive transcription factors such as MRTFA and SRF contribute to both upregulation of morphological genes as well as suppression of mitochondrial programs.

Identifiants

pubmed: 32047213
doi: 10.1038/s41598-020-59284-w
pii: 10.1038/s41598-020-59284-w
pmc: PMC7012923
doi:

Substances chimiques

Extracellular Matrix Proteins 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

2380

Subventions

Organisme : NIDDK NIH HHS
ID : R01 DK117161
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM127625
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK100422
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK046200
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK117163
Pays : United States

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Auteurs

Jessica E C Jones (JEC)

Department of Biochemistry, Boston University School of Medicine, 72 East Concord Street, Boston, MA, 02118, USA.
Internal Medicine Research Unit, Worldwide Research, Development and Medical, Pfizer Inc, 1 Portland Street, Cambridge, MA, 02139, USA.

Nabil Rabhi (N)

Department of Biochemistry, Boston University School of Medicine, 72 East Concord Street, Boston, MA, 02118, USA.

Joseph Orofino (J)

Department of Biochemistry, Boston University School of Medicine, 72 East Concord Street, Boston, MA, 02118, USA.

Ramya Gamini (R)

Internal Medicine Research Unit, Worldwide Research, Development and Medical, Pfizer Inc, 1 Portland Street, Cambridge, MA, 02139, USA.

Valentina Perissi (V)

Department of Biochemistry, Boston University School of Medicine, 72 East Concord Street, Boston, MA, 02118, USA.

Cecile Vernochet (C)

Internal Medicine Research Unit, Worldwide Research, Development and Medical, Pfizer Inc, 1 Portland Street, Cambridge, MA, 02139, USA.

Stephen R Farmer (SR)

Department of Biochemistry, Boston University School of Medicine, 72 East Concord Street, Boston, MA, 02118, USA. sfarmer@bu.edu.

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