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Liver macrophages inhibit the endogenous antioxidant response in obesity-associated insulin resistance [miRNA-Seq]

ABSTRACT: Liver macrophages inhibit the endogenous antioxidant response in obesity-associated insulin resistance [miRNA-Seq]

PROVIDER: PRJNA549080 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9307630.fastq.gz	Fastqsanger.gz
	SRR9307640.fastq.gz	Fastqsanger.gz
	SRR9307631.fastq.gz	Fastqsanger.gz
	SRR9307641.fastq.gz	Fastqsanger.gz
	SRR9307632.fastq.gz	Fastqsanger.gz

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Liver macrophages inhibit the endogenous antioxidant response in obesity-associated insulin resistance

Project description:Liver macrophages inhibit the endogenous antioxidant response in obesity-associated insulin resistance

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Liver macrophages inhibit the endogenous antioxidant response in obesity-associated insulin resistance [RNA-Seq]

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Liver macrophages inhibit the endogenous antioxidant response in obesity-associated insulin resistance [RNA-Seq]

Project description:Liver Macrophages exacerbate oxidative stress induced by hepatic steatosis in obesity by blocking the endogenous anti-oxidant response.

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Liver macrophages inhibit the endogenous antioxidant response in obesity-associated insulin resistance [miRNA-Seq]

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COMMD10-deficiency in adipose tissue macrophages attenuates obesity and insulin resistance by boosting mitochondrial and antioxidant functions

Project description:During obesity, adipose tissue macrophages (ATM) colonize the white adipose tissue (WAT), where they adapt inflammatory and metabolically activated phenotypes. Here, we demonstrate that COMMD10 is a key regulator of macrophage oxidative capacity in response to chronic caloric excess. Mice with COMMD10-deficiency targeted to macrophages were fed with high-fat-diet (HFD) for 12 weeks. They gained less weight despite similar food intake, and showed improved systemic metabolic indices, sustained adipose tissue insulin sensitivity, increased lipolysis and reduced adipocyte hypertrophy and liver steatosis. COMMD10-deficient ATM directly improved insulin sensitivity and increase lipolysis in co-cultured adipocytes. COMMD10-deficient ATM exhibited increased oxidative respiration and mitochondrial membrane potential after short term (five weeks) and chronic (12 weeks) HFD. Their oxidative respiration was fueled by both glucose and lipids. They better adapted to mitochondrial activation by upregulating NRF2-dependent antioxidant transcriptional module. their increase in mitochondrial activity was furthered supported by COMMD10 modulation of cellular copper-iron balance and interaction with various oxidative phosphorylation related proteins. Our study illuminates COMMD10 as a pivotal regulator of mitochondrial energy production in ATM during constant energy surplus.

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COMMD10-deficiency in adipose tissue macrophages attenuates obesity and insulin resistance by boosting mitochondrial and antioxidant functions

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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.

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The inflammasome is a central player in the induction of obesity and insulin resistance

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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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