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KLF10 deficiency in CD4+ T cells triggers obesity and insulin resistance

ABSTRACT: KLF10 deficiency in CD4+ T cells triggers obesity and insulin resistance

PROVIDER: PRJNA588090 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10409081_1.fastq.gz	Fastqsanger.gz
	SRR10409081_2.fastq.gz	Fastqsanger.gz
	SRR10409082_1.fastq.gz	Fastqsanger.gz
	SRR10409082_2.fastq.gz	Fastqsanger.gz
	SRR10409083_1.fastq.gz	Fastqsanger.gz

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KLF10 deficiency in CD4+ T cells triggers obesity and insulin resistance

Project description:Gene expression profiling of CD4+ T regs from WT and CD4-KLF10-KO mice on a high-fat diet.

2020-11-06 | GSE139977 | GEO

KLF10 Deficiency in CD4<sup>+</sup> T Cells Triggers Obesity, Insulin Resistance, and Fatty Liver.

Project description:CD4+ T cells regulate inflammation and metabolism in obesity. An imbalance of CD4+ T regulatory cells (Tregs) is critical in the development of insulin resistance and diabetes. Although cytokine control of this process is well understood, transcriptional regulation is not. KLF10, a member of the Kruppel-like transcription factor family, is an emerging regulator of immune cell function. We generated CD4+-T-cell-specific KLF10 knockout (TKO) mice and identified a predisposition to obesity, insulin resistance, and fatty liver due to defects of CD4+ Treg mobilization to liver and adipose tissue depots and decreased transforming growth factor β3 (TGF-β3) release in vitro and in vivo. Adoptive transfer of wild-type CD4+ Tregs fully rescued obesity, insulin resistance, and fatty liver. Mechanistically, TKO Tregs exhibit reduced mitochondrial respiration and glycolysis, phosphatidylinositol 3-kinase (PI3K)-Akt-mTOR signaling, and consequently impaired chemotactic properties. Collectively, our study identifies CD4+ T cell KLF10 as an essential regulator of obesity and insulin resistance by altering Treg metabolism and mobilization.

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FOXO1-KLF10 reinforcing loop promotes adipose lipolysis to facilitate exercise-induced anti-obesity effect in male mice

Project description:Exercise is recognized to be an effective way in the combat against obesity and related metabolic disorders, but the underlying mechanism is incompletely understood. Krüppel-like factor 10 (KLF10) is a transcription factor participating in diverse biological processes. KLF10 expression is abundant in adipose tissue, but its role in obesity is not well defined. Here, we show that exercise could facilitate adipocyte-derived KLF10 expression via the SIRT1/FOXO1 pathway. Adipocyte-specific knockout of KLF10 (KLF10AKO) blunts exercise-promoted white adipose browning, energy expenditure, fat loss, and glucose tolerance in diet-induced obese (DIO) mice. On the contrary, adipocyte-specific transgenic expression of KLF10 in mice (KLF10ATG) enhanced the abovementioned metabolic benefits induced by exercise. Mechanistically, KLF10 interacts with FOXO1 and facilitates the recruitment of KDM4A to form a ternary complex on the promoter regions of the Pnpla2 and Lipe genes to promote the expression of these key lipolytic genes, therefore facilitating lipolysis to defend against DIO in mice. As a newfound downstream effector responding to exercise, adipose KLF10 could act as a potential target in the fight against obesity

2024-08-25 | GSE269020 | GEO

KLF10 deficiency in CD4+ T cells promotes atherosclerosis progression by altering macrophage dynamics

Project description:Gene expression profiling of aortic tissue from WT and CD4-KLF10-KO mice injected once with the AAV-PCSK9D377Y gain-of-function transgene and placed on high cholesterol diet.

2023-02-03 | GSE196585 | GEO

Murine Pancreatic Cancer Cells: KLF10 wild type vs KLF10 knockout

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KLF10 targets

Project description:Experiment comparing the liver transcriptome from wild type and KLF10 deficient mice

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MOF haploinsufficiency triggers diet-induced obesity resistance

Project description:MOF haploinsufficiency triggers diet-induced obesity resistance

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Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity

Project description:Trim28 Haploinsufficiency Triggers Bi-stable Epigenetic Obesity

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Acetytransferase P300 impairs insulin signaling in obesity

Project description:Insulin resistance is the hallmark of obese and type 2 diabetes patients. Defective insulin sensitivity in the liver results in increased glucsoe production, which is the major cause of hyperglycemia in diabetic patients. Increased lipopolysaccharide (LPS) leakage from the gut of diet-induced obesity causes insulin resisitance; moreover, activation of deacetylase Sirtuin1 restore insulin sensitivity in obesity. However, the mechanism resulting in insulin resistance by LPS remains poorly understood. Here, we show that Ep300 (P300) harboring an intrinsic acetyltransferase activity was rapidly induced in the liver of animals fed a high-fat diet, and the induction of Ep300 is through LPS-stimulated activation of ER stress. Induced Ep300 impairs insulin signaling by acetylating mediators in insulin signaling. Inhibition of P300 acetyltransferase activity improves insulin signaling. Thus, Ep300 acetyltransferase activity is a therapeutic target.

2017-05-08 | GSE86108 | GEO

IL-37 protects against obesity-induced inflammation and insulin resistance

Project description:Cytokines of the IL-1 family are important modulators of obesity-induced inflammation and the development of systemic insulin resistance. Here, we report that IL-37, a newly-described antiinflammatory member of the IL-1 family, affects obesity-induced inflammation and insulin resistance. IL-37 transgenic mice (IL-37tg) did not develop an obese phenotype in response to a high-fat diet (HFD). Unlike WT mice, IL-37tg mice exhibited reduced numbers of adipose tissue macrophages and preserved glucose tolerance and insulin sensitivity after 16 weeks of HFD. A short-term HFD intervention revealed that the IL-37-mediated improvement in glucose tolerance is independent of bodyweight. IL-37tg mice manifested a beneficial metabolic profile with higher circulating levels of the anti-inflammatory adipokine adiponectin. In vitro treatment of differentiating adipocytes with recombinant IL-37 reduced adipogenesis. The beneficial effects of recombinant IL-37 involved activation of AMPK signaling. In humans, steady-state IL-37 adipose tissue mRNA levels were positively correlated with insulin sensitivity, lower adipose tissue levels of leptin and a lower inflammatory status of the adipose tissue. These findings reveal IL-37 as an important anti-inflammatory modulator during obesity-induced inflammation and insulin resistance in both mice and humans and suggest that IL-37 is a potential target for the treatment of obesity-induced insulin resistance and type 2 diabetes. Gene arrays were performed on epidydimal white adipose tissue samples from wild type and human IL37-overexpressing transgenic mice fed a high fat diet for 16 weeks.

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