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Cited by 62Peroxisome Proliferator-Activated ReceptorsAdipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and Metabolism

Adipocytes fail to maintain cellular identity during obesity due to reduced PPARγ activity and elevated TGFβ-SMAD signaling

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Roh, Hyun Cheol, Kumari, Manju, Taleb, Solaema, Tenen, Danielle, Jacobs, Christopher, Lyubetskaya, Anna, Tsai, Linus T.-Y., Rosen, Evan D.·2020·Molecular Metabolism
DOI 10.1016/j.molmet.2020.101086PMC PMC7559520
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Abstract

OBJECTIVE: Obesity due to overnutrition causes adipose tissue dysfunction, which is a critical pathological step on the road to type 2 diabetes (T2D) and other metabolic disorders. In this study, we conducted an unbiased investigation into the fundamental molecular mechanisms by which adipocytes transition to an unhealthy state during obesity. METHODS: We used nuclear tagging and translating ribosome affinity purification (NuTRAP) reporter mice crossed with Adipoq-Cre mice to determine adipocyte-specific 1) transcriptional profiles (RNA-seq), 2) promoter and enhancer activity (H3K27ac ChIP-seq), 3) and PPARγ cistrome (ChIP-seq) profiles in mice fed chow or a high-fat diet (HFD) for 10 weeks. We also assessed the impact of the PPARγ agonist rosiglitazone (Rosi) on gene expression and cellular state of adipocytes from the HFD-fed mice. We integrated these data to determine the transcription factors underlying adipocyte responses to HFD and conducted functional studies using shRNA-mediated loss-of-function approaches in 3T3-L1 adipocytes. RESULTS: Adipocytes from the HFD-fed mice exhibited reduced expression of adipocyte markers and metabolic genes and enhanced expression of myofibroblast marker genes involved in cytoskeletal organization, accompanied by the formation of actin filament structures within the cell. PPARγ binding was globally reduced in adipocytes after HFD feeding, and Rosi restored the molecular and cellular phenotypes of adipocytes associated with HFD feeding. We identified the TGFβ1 effector protein SMAD to be enriched at HFD-induced promoters and enhancers and associated with myofibroblast signature genes. TGFβ1 treatment of mature 3T3-L1 adipocytes induced gene expression and cellular changes similar to those seen after HFD in vivo, and knockdown of Smad3 blunted the effects of TGFβ1. CONCLUSIONS: Our data demonstrate that adipocytes fail to maintain cellular identity after HFD feeding, acquiring characteristics of a myofibroblast-like cell type through reduced PPARγ activity and elevated TGFβ-SMAD signaling. This cellular identity crisis may be a fundamental mechanism that drives functional decline of adipose tissues during obesity.

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  • Adipocytes undergo hypertrophy, an increase in cell size, during obesity, accompanied by significant cytoskeletal rearrangement.

    “Adipocytes undergo hypertrophy, an increase in cell size, during obesity, accompanied by significant cytoskeletal rearrangement (Roh et al., 2020).”

    From Robust single-nucleus RNA sequencing reveals depot-specific cell population dynamics in adipose tissue remodeling during obesity (2025) · cites this paper as Roh et al., 2020

    The Results section, “Adipocytes undergo remodeling of cytoskeletal organizations on an HFD” (page unavailable), reports substantially denser and more complex actin filaments in adipocytes from high-fat-diet mice, supporting cytoskeletal rearrangement. The Introduction describes adipose-tissue expansion during obesity, but the passages found do not establish that the adipocytes themselves increased in size; that hypertrophy component is not supported by our copy. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • This aligns with earlier findings, which demonstrated the failure of adipocytes to maintain their identity during obesity.

    “This aligns with our earlier findings, which demonstrated the failure of adipocytes to maintain their identity during obesity (Roh et al., 2020).”

    From Robust single-nucleus RNA sequencing reveals depot-specific cell population dynamics in adipose tissue remodeling during obesity (2025) · cites this paper as Roh et al., 2020

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Authors
Roh, H. C., Kumari, M., Taleb, S., Tenen, D., Jacobs, C., Lyubetskaya, A., Tsai, L. T.-Y., & Rosen, E. D.
Affiliations
  • Broad Institute (US)
  • Beth Israel Deaconess Medical Center (US)
  • Indiana University Indianapolis (US)
Corresponding author
  • Roh, Hyun Cheol
  • Rosen, Evan D.
ORCID
Venue
Molecular Metabolism
Publisher
Elsevier BV
Published
2020-12
Volume
42
Pages
101086
ISSN
2212-8778 (ISSN-L)
DOI
10.1016/j.molmet.2020.101086
PMC
PMC7559520
OpenAlex
W3090056912
Cited by
62
References
8
Citations by year
2026: 11 · 2025: 17 · 2024: 17 · 2023: 6 · 2022: 8 · 2021: 3
FWCI
1.38
Type
journal article
Language
en
Open access
Licence
Locations
  • Molecular Metabolism (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Purdue University Indianapolis (Indiana University) (submittedVersion, cc-by-nc-nd)
  • PMC
Funders
National Institutes of Health
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords
obesity, PPARγ, TGF-β1, Smad signaling, high-fat diet, rosiglitazone, adipose tissue dysfunction, type 2 diabetes, enhancer activity, actin cytoskeleton, Smad3
MeSH terms
Rosiglitazone, Adipose Tissue, Animals, Cell Differentiation, Humans, Insulin, Insulin Resistance, Mice, Inbred C57BL, Mice, Transgenic, Obesity, Signal Transduction, Transforming Growth Factor beta, Adipocytes, 3T3-L1 Cells, PPAR gamma, Adipogenesis, Mice, Smad Proteins, Diet, High-Fat

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