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Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism [ChIP-seq]

ABSTRACT: Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism [ChIP-seq]

PROVIDER: PRJNA531178 | ENA |

REPOSITORIES: ENA

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Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism

Project description:Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism

| PRJNA531175 | ENA

Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism [HFD]

Project description:Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism [HFD]

| PRJNA531177 | ENA

Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism [preadipocytes]

Project description:Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism [preadipocytes]

| PRJNA531180 | ENA

Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism [preadipocytes]

Project description:We generated a Tcf7l2 F/F mouse and harvested preadipocytes rom these mice, immortalized them, and then transduced them with a retroviral vector containing CreERT2 and , differentiated them, performed ChIP-seq, and RNA-seq. We also generated and adipsoe specific knockout mouse where we crossed our Tcf7 F/Fmouse with an Adiponectin-Cre mice and performed RNA-seq on the inguimal white adipose tissue after 16 weeks of high fat diet, 65% Conclusions: Our study shows that knocking of Tcf7l2 results in enhanced adipocyte differentiation

2019-08-01 | GSE129404 | GEO

Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism [HFD]

Project description:We generated a Tcf7l2 F/F mouse and harvested preadipocytes from these mice, immortalized them, and then transduced them with a retroviral vector containing CreERT2 and , differentiated them, performed ChIP-seq, and RNA-seq. We also generated an adipose specific knockout mouse where we crossed our Tcf7 F/Fmouse with an Adiponectin-Cre mice and performed RNA-seq on the inguinal white adipose tissue after 16 weeks of high fat diet, 65% Conclusions: Adipsose selective deletion of Tcf7l2 led to hypertrophic inguinal white adipose tissue and impaired glucose metabolsim with transcripts involved in lipid and glucose metabolsim being altered.

2019-08-01 | GSE129402 | GEO

Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism [ChIP-seq]

2019-08-01 | GSE129403 | GEO

The developmental and metabolic roles of the diabetes candidate gene TCF7L2 in adipose tissue

Project description:The gene encoding for transcription factor 7-like 2 (TCF7L2) is the strongest type 2 diabetes (T2DM) candidate gene discovered to date. While its association with T2DM has been replicated in most populations worldwide, the molecular and physiological mechanisms that underlie this association remain largely unknown. As a key transcriptional effector of the Wnt/β-catenin signaling pathway, we hypothesized that TCF7L2 plays an important role in the development and function of adipocytes. Using a combination of in vitro and in vivo approaches, we show that TCF7L2 is critical for proper adipogenesis and that inactivating TCF7L2 mediated transcription by removing its DNA binding domain in mature adipocytes leads to whole-body glucose intolerance and hepatic insulin resistance in mice. This effect is secondary to an increase in subcutaneous adipose tissue mass caused by adipocyte hypertrophy that worsens with age and with high-fat feeding. Finally, in humans with adipocyte insulin resistance we demonstrate that TCF7L2 expression is downregulated, highlighting the translational importance of our findings. In summary our data indicate that TCF7L2 is an important mediator of adipocyte biology and has key roles in adipose tissue development and function.

2018-02-07 | GSE95029 | GEO

Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired glucose metabolism.

Project description: Not available

| S-EPMC6531814 | biostudies-literature

Genome-wide maps of Dnmt1-dependent DNA methylome in adipocytes

Project description:White adipose tissue (WAT) is a key regulator of systemic energy metabolism, and impaired WAT plasticity characterized by enlargement of preexisting adipocytes associates with WAT dysfunction, obesity and metabolic complications. However, the mechanisms that retain proper adipose tissue plasticity required for metabolic fitness are unclear. Here, we comprehensively showed that adipocyte-specific DNA methylation, manifested in enhancers and CTCF sites, directs distal enhancer-mediated transcriptomic features required to conserve metabolic functions of white adipocytes. Particularly, genetic ablation of adipocyte Dnmt1, the major methylation writer, led to increased adiposity characterized by increased adipocyte hypertrophy along with reduced expansion of adipocyte precursors (APs). These effects of Dnmt1 deficiency provoked systemic hyperlipidemia and impaired energy metabolism both in lean and obese mice. Mechanistically, Dnmt1 deficiency abrogated mitochondrial bioenergetics by inhibiting mitochondrial fission and promoted aberrant lipid metabolism in adipocytes, rendering adipocyte hypertrophy and WAT dysfunction. Dnmt1-dependent DNA methylation prevented aberrant CTCF binding and, in turn, sustained the proper chromosome architecture to permit interactions between enhancer and dynamin-related protein gene Drp1 in adipocytes. Also, adipose DNMT1 expression inversely correlated with adiposity and markers of metabolic health, but positively correlated with AP-specific markers in obese human subjects. Thus, these findings support strategies utilizing Dnmt1 action on mitochondrial bioenergetics in adipocytes to combat obesity and related metabolic pathology.

2021-03-24 | GSE158944 | GEO

Targeted deletion of Tcf7l2 in adipocytes promotes adipocyte hypertrophy and impaired gluose metabolism

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-08-01 | GSE129405 | GEO