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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE132800 | GEO | 2019/06/21

REPOSITORIES: GEO

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

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

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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 [miRNA-Seq]

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

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

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Inducible hepatic expression of CREBH mitigates diet-induced obesity, insulin resistance and hepatice steatosis in mice.

Project description:Cyclic AMP-responsive element-binding protein H (CREBH, encoded by Creb3l3) is a transcription factor that regulates the expression of genes that control lipid and glucose metabolism, as well as inflammation. CREBH is upregulated in the liver under conditions of overnutrition, and mice globally lacking the gene (CREBH-/-) are highly susceptible to diet-induced obesity, insulin resistance (IR) and hepatic steatosis. The net protective effects of CREBH have been attributed in large part to the activities of Fibroblast growth factor (Fgf)-21 (Fgf21), a target gene that promotes weight loss, improves glucose homeostasis and reduces hepatic lipid accumulation. To explore the possibility that activation of the CREBH-Fgf21 axis could ameliorate established effects of high fat feeding, we generated an inducible transgenic hepatocyte-specific CREBH overexpression mouse model (Tg-rtTA). Acute overexpression of CREBH in livers of Tg-rtTA mice effectively reversed diet-induced obesity, IR and hepatic steatosis. These changes were associated with increased activities of thermogenic brown and beige adipose tissues in Tg-rtTA mice, leading to reductions in fat mass, along with enhanced insulin sensitivity and glucose tolerance. Genetically silencing of Fgf21 in Tg-rtTA mice abrogated the CREBH-mediated reductions in body weight loss, but only partially reversed the observed improvements in glucose metabolism. These findings reveal that the protective effects of CREBH activation may be leveraged to mitigate diet-induced obesity and associated metabolic abnormalities in both Fgf21-dependent and -independent pathways.

2021-04-30 | GSE173548 | GEO

Glucose-dependent insulinotropic polypeptide ameliorates obesity and insulin resistance by attenuating S100A8/9 in myeloid cells

Project description:Our data mark GIP as a beneficial immunoregulator during obesity and suggest a novel untapped therapeutic potential for specific targeted GIP analogs. Emerging studies suggest that glucose-dependent insulin tropic polypeptide (GIP) affect obesity-associated inflammation. Yet, whether GIP can directly regulate immune cell activity and the respective metabolic consequences remained unknown. Here, we targeted GIP-receptor-deficiency to immune cells using bone marrow (BM) chimerism approach and the reconstituted chimeric mice were subjected to a high fat diet (HFD) regimen. Mice reconstituted with Gipr-/- BM gained significantly more weight, despite similar food consumption. This was accompanied by increased epididymal adipose tissue (epiWAT) mass, adipocyte hypertrophy, enhanced hepatic steatosis, insulin resistance and significant myelopoiesis in the circulation, epiWAT and inguinal adipose tissue (ingWAT). In accordance these mice also exhibited reduced energy expenditure and ingWAT beiging. Mechanistically, impaired GIP-governed regulation of S100A8/9 in myeloid cells was responsible for the perturbed energy homeostasis, increased insulin resistance and intensified inflammatory response under nutrient overload. Collectively, our results outline a beneficial immunoregulatory role for GIP in immune cells during obesity.

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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.

2015-05-18 | E-GEOD-58952 | biostudies-arrayexpress

Nuclear receptor, RORa plays a critical role in obesity-associated inflammation, hepatic steatosis, and insulin resistance

Project description:We demonstrated that RORa-deficient staggerer mice (RORasg/sg) fed with a high fat diet (HFD) showed reduced adiposity and hepatic triglyceride levels compared to wild type (WT) littermates and were resistant to the development of hepatic steatosis, adipose-associated inflammation, and insulin resistance. Gene expression profiling showed that many genes involved in triglyceride synthesis and storage, including Cidec, Cidea, and Mogat1, were expressed at much lower levels in liver of RORasg/sg mice. In addition to reduced lipid accumulation, inflammation was greatly diminished in white adipose tissue (WAT) of RORasg/sg mice fed with a HFD. The infiltration of macrophages and the expression of many immune-response and pro-inflammatory genes, including those encoding various chemo/cytokines, toll-like receptors, and TNF signaling proteins, were significantly reduced in RORasg/sg WAT. Moreover, RORasg/sg mice fed with a HFD were protected from the development of insulin resistance. Together, these results indicate that RORa plays a critical role in the regulation of several aspects of metabolic syndrome. Therefore, RORa may provide a novel therapeutic target in the management of obesity and associated metabolic diseases. Liver and white adipose tissue (WAT) total RNAs were purified from 5 WT and 5 RORasg/sg (natural deletion of RORa gene in mice) mice fed with a high fat diet for 6 weeks. Then samples were applied on Agilent mouse genome chip.

2011-04-30 | E-GEOD-23736 | biostudies-arrayexpress

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