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GPR120 mediates high-fat diet induced obesity

ABSTRACT: Analysis of GPR120 which play roles for the fatty acid sensor in adipose tissue. Results provide insight into the transcriptional effects caused by the loss of the GPR120 proteins and provide further insight into their functions.

ORGANISM(S): Mus musculus

PROVIDER: GSE32095 | GEO | 2012/02/22

SECONDARY ACCESSION(S): PRJNA147563

REPOSITORIES: GEO

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GPR120 mediates high-fat diet induced obesity

Project description:Analysis of GPR120 which play roles for the fatty acid sensor in adipose tissue. Results provide insight into the transcriptional effects caused by the loss of the GPR120 proteins and provide further insight into their functions. GPR120 KO mice and the corresponding wild-type with normal diet(ND) or high fat diet(HFD), were subjected to Affymetrix Mus musculus microarrays. Epididymal adipose tissue and liver were analyzed in triplicates.

2012-02-22 | E-GEOD-32095 | biostudies-arrayexpress

A novel GPR120-dependent pathway of control brown fat activation mediated by FGF21

Project description:Brown adipose tissue (BAT) thermogenesis and the browning of white adipose tissue are important components of energy expenditure. An RNAseq-based analysis of the mouse BAT transcriptome led us to identify GPR120 as a gene induced by thermogenic activation. GPR120, a G protein-coupled receptor binding unsaturated long-chain fatty acids, is known to mediate some beneficial metabolic actions of polyunsaturated fatty acids. We show that pharmacological activation of GPR120 induces BAT activity and promotes the browning of white fat in mice, whereas GRP120-null mice show impaired browning in response to cold. n-3 polyunsaturated fatty acids induce brown and beige adipocyte differentiation and thermogenic activation, and these effects require GPR120. GPR120 activation induces the release of fibroblast growth factor-21 (FGF-21) by brown and beige adipocytes and increases blood FGF21 levels. The effects of GPR120 activation are impaired in FGF21-null mice and cells. Thus, the lipid sensor GPR120 constitutes a novel pathway of brown fat activation and involves FGF21.

2016-12-12 | GSE77534 | GEO

Analysis of the differences in gene expression between wild type and Gpr120 knockout brown adipose tissue

Project description:The goals were to investigate differences in gene expression between wild type and Gpr120 knockout mouse interscapular brown adipose tissue

2018-01-18 | GSE97145 | GEO

A Gpr120 Selective Agonist Improves Insulin Resistance and Chronic Inflammation

Project description:We report that a high affinity, selective, small molecule Gpr120 agonist (cpdA), exerts potent anti-inflammatory effects on macrophages in vitro, and in obese mice in vivo. Gpr120 agonist treatment of high fat diet (HFD)/obese mice causes improved glucose tolerance, decreased hyperinsulinemia, increased insulin sensitivity and decreased hepatic steatosis. This suggests that Gpr120 agonists could become new insulin sensitizing drugs for the treatment of Type 2 diabetes and other human insulin resistant states in the future. Examination of effects of DHA and compound A on primary macrophages stimulated by LPS, 3 replicates for each condition

2014-06-07 | E-GEOD-58282 | biostudies-arrayexpress

A Gpr120 Selective Agonist Improves Insulin Resistance and Chronic Inflammation

2014-06-07 | GSE58282 | GEO

Next Generation Sequencing facilitates Quantitative Analysis of mouse CD4+ T cells affected by Gpr120

Project description:The goal of this study is to analyze the effect of Gpr120 in mouse CD4+ T cells.

2021-09-11 | GSE158782 | GEO

MicroRNA regulation of adipose tissue macrophages during high-fat diet-induced obesity.

Project description:We used microRNA microarrays to identify dysregulated microRNAs in macrophages isolated from adipose tissue of lean and obese mice.

2018-05-22 | GSE114736 | GEO

Transcriptional control of adipose tissue macrophages during high-fat diet-induced obesity.

Project description:We used transcriptome microarrays to identify gene expression changes in macrophages isolated from adipose tissue of lean and obese mice.

2018-05-22 | GSE114735 | GEO

Antiretroviral therapy potentiates high-fat diet induced obesity and glucose intolerance

Project description:Background Breakthroughs in HIV treatment, especially antiretroviral therapy (ART), have massively reduced mortality. However, ART-treated individuals display elevated rates of obesity, diabetes, and cardiovascular disease, collectively known as metabolic syndrome. These co-morbidities represent a considerable threat to long-term survival and quality of life. Previous studies have shown that high-fat feeding induces persistent low-grade systemic and adipose tissue inflammation contributing to insulin resistance and metabolic dysregulation via adipose-infiltrating macrophages. Methods and Results Studies herein test the hypothesis that ART potentiates the inflammatory effects of a high-fat diet (HFD). C57Bl/6J mice on a HFD or standard chow containing ART or vehicle, were subjected to functional metabolic testing, RNA-sequencing of epididymal white adipose tissue (eWAT), and array-based kinomic analysis of eWAT-infiltrating macrophages. ART-treated mice on a HFD displayed fat mass accumulation, impaired glucose tolerance, and potentiated insulin resistance. Gene set enrichment and kinomic array analyses revealed a pro-inflammatory transcriptional signature depicting granulocyte migration and activation. Conclusions The current study reveals a HFD-ART interaction that increases inflammatory transcriptional pathways in eWAT consistent with macrophage infiltration, resulting in impaired glucose metabolism, energy balance, and metabolic dysfunction.

2018-09-14 | GSE110035 | GEO

High-Fat Diet-Induced Complement Activation Mediates Intestinal Inflammation and Neoplasia, Independent of Obesity.

Project description:Obesity and related metabolic disturbances are closely associated with pathologies that represent a significant burden to global health. Epidemiological and molecular evidence links obesity and metabolic status with inflammation and increased risk of cancer. Here, using a mouse model of intestinal neoplasia and strains that are susceptible or resistant to diet-induced obesity, it is demonstrated that high-fat diet-induced inflammation, rather than obesity or metabolic status, is associated with increased intestinal neoplasia. The complement fragment C5a acts as the trigger for inflammation and intestinal tumorigenesis. High-fat diet induces complement activation and generation of C5a, which in turn induces the production of proinflammatory cytokines and expression of proto-oncogenes. Pharmacological and genetic targeting of the C5a receptor reduced both inflammation and intestinal polyposis, suggesting the use of complement inhibitors for preventing diet-induced neoplasia.ImplicationsThis study characterizes the relations between diet and metabolic conditions on risk for a common cancer and identifies complement activation as a novel target for cancer prevention. Mol Cancer Res; 14(10); 953-65. ©2016 AACR.

| S-EPMC5330314 | biostudies-literature

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