Expression of clock gene<i>Dbp</i>in omental and mesenteric adipose tissue in patients with type 2 diabetes

Ushijima, Kazuo; Suzuki, Chisato; Kitamura, Hiroko; Shimada, Ken; Kawata, Hirotoshi; Tanaka, Akira; Horie, Hisanaga; Hosoya, Yoshinori; Imai, Yasushi; Yamashita, Chikamasa; Fujimura, Akio

doi:10.1136/bmjdrc-2020-001465

Cited by 8 publications

(7 citation statements)

References 37 publications

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“…We identified Dbp and its homologs Tef and Hlf as potential master regulators of the upregulated rhythmic pathway. Dbp is a transcription factor with expression under circadian control ( Zvonic et al, 2006 ) and has been reported to improve insulin sensitivity and enhance adipogenesis in pre-adipocytes of vWAT in mice and humans ( Suzuki et al, 2019 ; Ushijima et al, 2020 ). Taken together, we hypothesize that training-induced increases in circadian rhythm gene expression via Dbp may contribute to hyperplasia in WAT.…”

Section: Discussionmentioning

confidence: 99%

Single-cell dissection of the obesity-exercise axis in adipose-muscle tissues implies a critical role for mesenchymal stem cells

Yang

Vamvini²,

Nigro³

et al. 2022

Cell Metabolism

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Section: Discussionmentioning

confidence: 99%

Single-cell dissection of the obesity-exercise axis in adipose-muscle tissues implies a critical role for mesenchymal stem cells

Yang

Vamvini²,

Nigro³

et al. 2022

Cell Metabolism

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“…Induction of Dbp was reported to ameliorate insulin sensitivity via direct binding to the promoter region of Pparg, driving mRNA expression of a splicing variant of Pparg (Ppar-γ1sv), and enhancing adipogenesis in preadipocytes from ob/ob mice vWAT 75 . Promoter activity of Dbp as reflected by histone H3 lysine 9 acetylation (H3K9ac) levels, and Dbp and Pparg expression in omental adipose tissue, were reported to be decreased in patients with T2D 76 . Our results suggest that exercise-induced circadian rhythm gene expression changes regulated by Dbp may contribute to adipogenesis of ASCs in WAT.…”

Section: Discussionmentioning

confidence: 99%

Single-cell dissection of obesity-exercise axis in adipose-muscle tissues

Yang

Vamvini

Nigro

et al. 2021

Preprint

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Regular physical exercise has long been recognized to reverse the effects of diet-induced obesity, but the molecular mechanisms mediating these multi-tissue beneficial effects remain uncharacterized. Here, we address this challenge by studying the opposing effects of exercise training and high-fat diet at single-cell, deconvolution and tissue-level resolutions across 3 metabolic tissues. We profile scRNA-seq in 204,883 cells, grouped into 53 distinct cell subtypes/states in 22 major cell types, from subcuta-neous and visceral white adipose tissue (WAT), and skeletal muscle (SkM) in mice with diet and exercise training interventions. With a great number of mesenchymal stem cells (MSCs) profiled, we compared depot-specific adipose stem cell (ASC) states, and defined 7 distinct fibro-adipogenic progenitor (FAP) states in SkM including discovering and validating a novel CD140+/CD34+/SCA1-FAP population. Exercise- and obesity-regulated proportion, transcriptional and cell-cell interaction changes were most strongly pronounced in and centered around ASCs, FAPs, macrophages and T-cells. These changes reflected thermogenesis-vs-lipogenesis and hyperplasia-vs-hypertrophy shifts, clustered in pathways including extracellular matrix remodeling and circadian rhythm, and implicated complex single- and multi-tissue communication including training-associated shift of a cytokine from binding to its decoy receptor on ASCs to true receptor on M2 macrophages in vWAT. Overall, our work provides new insights on the metabolic protective effects of exercise training, uncovers a previously-underappreciated role of MSCs in mediating tissue-specific and multi-tissue effects, and serves as a model for multitissue single-cell analyses in physiologically complex and multifactorial traits exemplified by obesity and exercise training.

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“…Increased H3K9me3 in the Slc2a4 promoter could reduce the expression of GLUT4, encoded by Slc2a4, which contributes to glycemic impairment in T2D (15). Acetylation of H3K9 at the promoter region of clock gene Dbp and DBP mRNA expression in omental adipose tissue, a compartment related to the mechanism of T2D, was significantly lower in T2D patients (112).…”

Section: Type 2 Diabetesmentioning

confidence: 99%

Role of Histone Post-Translational Modifications in Inflammatory Diseases

et al. 2022

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Inflammation is a defensive reaction for external stimuli to the human body and generally accompanied by immune responses, which is associated with multiple diseases such as atherosclerosis, type 2 diabetes, Alzheimer’s disease, psoriasis, asthma, chronic lung diseases, inflammatory bowel disease, and multiple virus-associated diseases. Epigenetic mechanisms have been demonstrated to play a key role in the regulation of inflammation. Common epigenetic regulations are DNA methylation, histone modifications, and non-coding RNA expression; among these, histone modifications embrace various post-modifications including acetylation, methylation, phosphorylation, ubiquitination, and ADP ribosylation. This review focuses on the significant role of histone modifications in the progression of inflammatory diseases, providing the potential target for clinical therapy of inflammation-associated diseases.

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Expression of clock geneDbpin omental and mesenteric adipose tissue in patients with type 2 diabetes

Cited by 8 publications

References 37 publications

Single-cell dissection of the obesity-exercise axis in adipose-muscle tissues implies a critical role for mesenchymal stem cells

Single-cell dissection of the obesity-exercise axis in adipose-muscle tissues implies a critical role for mesenchymal stem cells

Single-cell dissection of obesity-exercise axis in adipose-muscle tissues

Role of Histone Post-Translational Modifications in Inflammatory Diseases

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