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Luteolin attenuates lipid dysregulation and insulin resistance thorough interplay of liver and adipose tissue in diet-induced obese mice

ABSTRACT: Analysis of effect of luteolin on lipid metabolism at gene expression level. The hypothesis tested in the present study was that luteolin treatment with obesogenic diet suppressed the hepatic lipogenesis pathways. Conversely, in adipose tissue, luteolin stimulated the lipogenesis pathway and it also simultaneously increased the expression of genes controlling lipolysis and TCA cycle. Results provide important information about the effect on diet-induced obesity and its metabolic complications.

ORGANISM(S): Mus musculus

PROVIDER: GSE54189 | GEO | 2014/09/01

SECONDARY ACCESSION(S): PRJNA235389

REPOSITORIES: GEO

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Luteolin attenuates lipid dysregulation and insulin resistance thorough interplay of liver and adipose tissue in diet-induced obese mice

Project description:Analysis of effect of luteolin on lipid metabolism at gene expression level. The hypothesis tested in the present study was that luteolin treatment with obesogenic diet suppressed the hepatic lipogenesis pathways. Conversely, in adipose tissue, luteolin stimulated the lipogenesis pathway and it also simultaneously increased the expression of genes controlling lipolysis and TCA cycle. Results provide important information about the effect on diet-induced obesity and its metabolic complications. Total RNA of liver and adipose tissues was obtained from normal diet, high-fat diet and luteolin added high-fat diet-fed mice and mRNA expression-associated with lipid metabolism was measured.

2014-09-01 | E-GEOD-54189 | biostudies-arrayexpress

Luteolin attenuates hepatic and adipocyte fibrosis and insulin resistance by targeting toll-like receptors signaling pathway in diet-induced obese mice

Project description:The flavonoid luteolin possess a variety of anti-inflammatory properties, but little has known about the detailed mechanisms linked to the anti-metabolic syndrome action of luteolin based on the integration of the transcriptional profile and the phenotype biomarkers. The aim of this study was to investigate the protective role of luteolin on inflammation-mediated metabolic diseases, focusing on its role in modulating toll-like receptor (TLR) signaling pathway triggered up-regulation of pro-inflammatory cytokines. Above all, it provides novel insights into the effect of luteolin on the link among adiposopathy, insulin resistance, hepatic steatosis and fibrosis. C57BL/6J mice were fed a normal, high-fat, and high-fat + 0.005% (w/w) luteolin diet for 16 weeks. In this study, (a) luteolin treatment resulted in an improvement in chronic low-grade inflammation by modulating TLR-signaling pathway resulting in reduced pro-inflammatory cytokines and macrophage accumulation; (b) there is a positive relationship of TLR5, MKK4/7, p38 and JNK-related gene expressions and lipogenesis in luteolin-treated obese mice, which is linked to an attenuation of hepatic lipotoxicity with an increased hepatic anti-oxidant system; (c) luteolin prevented hepatic and adipocyte fibrosis by decreasing ECM accumulation and cathepsin gene expressions; (d) Emr1 and Ccl7 genes, important markers inducing low-grade inflammation, are affected by advancing age as well as body weight, and luteolin treatment normalized those gene expressions; (e) luteolin treatment improved insulin resistance by normalizing pancreatic islet dysfunction, and differentially modulating the plasma GLP-1 and GIP levels. Taken together, luteolin ameliorates the deleterious effects of diet-induced obesity and its comorbidity.

2018-03-06 | GSE111412 | GEO

Luteolin protects against obese sarcopenia in mice with high-fat diet-induced obesity by ameliorating inflammation and protein degradation in muscle

Project description:Although there are studies on obesity and sarcopenia, our understanding of obesity-mediated sarcopenia is insufficient. Additionally, no studies have investigated the application of luteolin in sarcopenia. We attempted to determine the effect of luteolin on obese sarcopenia in mice with high-fat diet (HFD)-induced obesity. Luteolin exerted suppressive effects on obesity, inflammation, and protein degradation in HFD-fed obese mice. Luteolin inhibited lipid infiltration into the muscle and decreased p38 and JNK activity and mRNA expression of inflammatory factors, such as TNFα, Tlr2, Tlr4, MCP1, and MMP2, in the muscle. Suppression of muscle inflammation by luteolin led to the inhibition of myostatin, FoxO, atrogin, and MuRF expression, which reduced protein degradation and improved muscle function. This is the first study to demonstrate that luteolin exerts a protective effect against obese sarcopenia, as its anti-obesity and anti-inflammatory activities inhibited protein degradation. Therefore, luteolin may be a useful supplement for prevention of obese sarcopenia.

2022-07-27 | GSE209778 | GEO

RNA sequencing Facilitates Quantitative Analysis of luteolin or quercetin on adipogenesis Transcriptomes

Project description:We report the use of transcriptome sequencing in the intervention of luteolin or quercetin in adipogenesis. We constructed the adipogenic differentiation model of mouse embryonic fibroblasts and obtained the differential genes of luteolin or quercetin regulating adipocyte differentiation by transcriptomic sequencing. We identified 2085 differentially expressed lipogenesis response genes, 181 luteolin response genes and 574 quercetin response genes. This study provides a framework for the network regulation mechanism of luteolin or quercetin inhibiting preadipocyte differentiation.

2023-12-01 | GSE219241 | GEO

Gene expression change in the liver by luteolin treatment in rats with nonalcoholic steatohepatitis

Project description:Gene expression change in the liver of connexin dominant negative transgenic (Tg) and wild-type (Wt) rats fed methionine-choline deficient diet (MCDD) or MCDD with luteolin for 12 weeks.

2017-12-31 | GSE68010 | GEO

miRNA array analysis following gefinitib/luteolin administration to PC-3 cells

Project description:To determine if any altered miRNA expression is actually involved in the growth inhibition and/or cell death induction by luteolin and/or gefitinib, we performed miR-array analysis using RNA from PC-3 cells after 24h of treatment with 60Î¼M luteolin and/or 60Î¼M gefitinib. PC-3 cells were treated for 24h with DMSO, 60Î¼M luteolin (Lut), 60Î¼M gefitinib (Gef) or their co-administration (Lut+Gef). Each sample was run in duplicate.

2014-06-29 | E-GEOD-53178 | biostudies-arrayexpress

The effect of senescent cells depletion in obese hearts

Project description:Obesity is a major contributor to metabolic and cardiovascular diseases. Senescence is a highly dynamic process activated by diverse stimuli and increased cellular senescence has been associated with age-related disorders. Here, we investigated the impact of cellular senescence in obesogenic diet-related metabolic and cardiac dysfunctions. An obesogenic diet induced an increase on body weight gain and adiposity, glucose intolerance, insulin resistance, dyslipidemia, and hepatic disorders in mice; however, these alterations were prevented by a senolytic cocktail (dasatinib and quercetin), which leads to removal of senescent cells. In addition, the elimination of senescent cells counteracted the activation of the senescent program and DNA damage in the white adipose tissue (WAT) induced by an obesogenic diet. Obese mice had an increase of the senescence-associated secretory phenotype (SASP) and DNA damage in the heart, cardiac hypertrophy, and diastolic dysfunction; however, the use of a senolytic combination abolished these myocardial alterations caused by an obesogenic diet. Transcriptomic analysis of the hearts revealed that obese mice exhibited a downregulation of genes associated with fatty acid metabolism, oxidative phosphorylation, PI3K AKT MTOR signaling, P53 pathway, and DNA repair; however, the treatment with senolytic cocktail induced an increase of these pathways in the heart. Collectively, these data suggest that obesogenic diet elicits WAT and cardiac senescence program in mice, and that targeting senescent cells may be a novel therapeutic strategy for attenuating obesity-related metabolic and cardiac disorders.

2024-12-19 | GSE264313 | GEO

Transcription profiling of mouse microglia reveals luteolin has anti-inflammatory and neurotrophic effects on microglia

Project description:Our aim was to identify genes that were differentially expressed in microglia stimulated with Lipopolysaccharide, Luteolin, or both. Affymetrix microarrays were used to analyze RNA samples Experiment Overall Design: RNA from control BV-2 cells, and cells treated for 24h with LPS, Luteolin, or LPS+Luteolin was analyzed with Affymetrix GeneChip Mouse Genome 430 2.0 Arrays. Biological triplicates were analyzed for each condition

2010-01-23 | E-GEOD-18740 | biostudies-arrayexpress

transcriptome analysis for luteolin or siVRK1 treated ovarian cancer cells

Project description:To investigate the function of Luteolin and siVRK1 on ovarian cancer, we use A2780 and ES2 cell lines treated with siCtrl, siVRK1, DMSO and luteolin to do the experiment. We then performed gene expression profiling analysis using data obtained from RNA-seq .

2022-09-07 | GSE212598 | GEO

Expression data from the hippocampus of LPS induced depression mice model treated with Luteolin

Project description:Gene expression profiling reveals a potential role of Luteolin in LPS induced depression model LPS depression induced mice were orally treated with luteolin (10 mg/kg body weight) once per day during 8 consecutive days. Microarray gene expression was conducted on mice hippocampal tissues. Two mice brains were used for each expermient . The Microarray gene expression was conducted on hipocampus from LPS depression induced mice model(LPS group), LPS depression induced mice model treated with luteolin(LPS+L group), Normal mice (PBS group) and Normal mice treated with luteolin (PBS+L).

2021-11-24 | GSE181285 | GEO

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