Anti-obesity effect of radix Angelica sinensis and candidate causative genes in transcriptome analyses of adipose tissues in high-fat diet-induced mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE89454 | GEO | 2016/11/15
SECONDARY ACCESSION(S): PRJNA352249
REPOSITORIES: GEO
Similar Datasets
Project description:Abstract: Obesity characterized by adiposity and ectopic fat accumulation is associated with the development of non-alcoholic fatty liver disease (NAFLD). Treatments that stimulate lipid utilization may prevent the development of obesity and comorbidities. This study evaluated the potential anti-obesogenic hepatoprotective effects of combined treatment with L-carnitine and nicotinamide riboside, i.e., components that can enhance fatty acid transfer across the inner mitochondrial membrane and increase nicotinamide adenine nucleotide (NAD+) levels, which are necessary for β-oxidation and the TCA cycle, respectively. Ldlr −/−.Leiden mice were treated with high-fat diet (HFD) supplemented with L-carnitine (LC; 0.4% w/w), nicotinamide riboside (NR; 0.3% w/w) or both (COMBI) for 21 weeks. L-carnitine plasma levels were reduced by HFD and normalized by LC. NR supplementation raised its plasma metabolite levels demonstrating effective delivery. Although food intake and ambulatory activity were comparable in all groups, COMBI treatment significantly attenuated HFD-induced body weight gain, fat mass gain (−17%) and hepatic steatosis (−22%). Also, NR and COMBI reduced hepatic 4-hydroxynonenal adducts. Upstream-regulator gene analysis demonstrated that COMBI reversed detrimental effects of HFD on liver metabolism pathways and associated regulators, e.g., ACOX, SCAP, SREBF, PPARGC1B, and INSR. Combination treatment with LC and NR exerts protective effects on metabolic pathways and constitutes a new approach to attenuate HFD-induced obesity and NAFLD.
2019-09-04 | GSE136821 | GEO
Project description:Auricularia auricula is a well-known traditional edible and medicinal fungus with high nutritional and pharmacological values, as well as metabolic and immunoregulatory properties. However, the exact mechanisms underlying the effects of Auricularia auricula polysaccharides (AAP) on obesity and related metabolic endpoints, including the role of the gut microbiota, remain insufficiently understood. To determine the mechanistic role of the gut microbiota in observed anti-obesogenic effects AAP, faecal microbiota transplantation (FMT) and pseudo germ-free mice model treated with antibiotics were also applied, together with 16S rRNA genomic-derived taxonomic profiling. HFD murine exposure to AAP thwarted weight-gains, reduced fat depositing, together with upregulating thermogenesis proteomic biomarkers within adipose tissue. These effects were associated with diminished intestine/bloodstream-borne lipid transportation, together with enhanced glucose tolerance. FMT administered in tandem with antibiotic treatment demonstrated the intestinal microbiota was necessary in deploying AAP anti-obesogenic functions. Intestine-dwelling microbial population assessments discovered AAP to enhance (in a selective manner) Papillibacter cinnamivorans, a commensal bacterium having reduced presence within HFD mice. Notably, HFD mice treated with oral formulations of Papillibacter cinnamivorans diminished obesity and was linked to decreased intestinal lipid transportation. Datasets from the present study show that AAP thwarted dietary-driven obesity and metabolism-based disorders through regulating intestinal lipid transportation, a mechanism that is dependent on the gut commensal Papillibacter cinnamivorans. These results indicated AAP and Papillibacter cinnamivorans as newly identified pre- and probiotics that could possibly serve as novel countermeasure against obesity.
2022-05-03 | GSE201951 | GEO
Project description:Auricularia auricula is a well-known traditional edible and medicinal fungus with high nutritional and pharmacological values, as well as metabolic and immunoregulatory properties. However, the exact mechanisms underlying the effects of Auricularia auricula polysaccharides (AAP) on obesity and related metabolic endpoints, including the role of the gut microbiota, remain insufficiently understood. To determine the mechanistic role of the gut microbiota in observed anti-obesogenic effects AAP, faecal microbiota transplantation (FMT) and pseudo germ-free mice model treated with antibiotics were also applied, together with 16S rRNA genomic-derived taxonomic profiling. HFD murine exposure to AAP thwarted weight-gains, reduced fat depositing, together with upregulating thermogenesis proteomic biomarkers within adipose tissue. These effects were associated with diminished intestine/bloodstream-borne lipid transportation, together with enhanced glucose tolerance. FMT administered in tandem with antibiotic treatment demonstrated the intestinal microbiota was necessary in deploying AAP anti-obesogenic functions. Intestine-dwelling microbial population assessments discovered AAP to enhance (in a selective manner) Papillibacter cinnamivorans, a commensal bacterium having reduced presence within HFD mice. Notably, HFD mice treated with oral formulations of Papillibacter cinnamivorans diminished obesity and was linked to decreased intestinal lipid transportation. Datasets from the present study show that AAP thwarted dietary-driven obesity and metabolism-based disorders through regulating intestinal lipid transportation, a mechanism that is dependent on the gut commensal Papillibacter cinnamivorans. These results indicated AAP and Papillibacter cinnamivorans as newly identified pre- and probiotics that could possibly serve as novel countermeasure against obesity.
2022-05-03 | GSE201950 | GEO
Project description:Auricularia auricula is a well-known traditional edible and medicial fungus with high nutritional and pharmacological values, as well as metabolic and immunoregulatory properties. However, the exact mechanisms underlying the effects of Auricularia auricula polysaccharides (AAP) on obesity and related metabolic endpoints, including the role of the gut microbiota, remain insufficiently understood. To determine the mechanistic role of the gut microbiota in observed anti-obesogenic effects AAP, faecal microbiota transplantation (FMT) and pseudo germ-free mice model treated with antibiotics were also applied, together with 16S rRNA genomic-derived taxonomic profiling. HFD murine exposure to AAP thwarted weight-gains, reduced fat depositing, together with upregulating thermogenesis proteomic biomarkers within adipose tissue. These effects were associated with diminished intestine/bloodstream-borne lipid transportation, together with enhanced glucose tolerance. FMT administered in tandem with antibiotic treatment demonstrated the intestinal microbiota was necessary in deploying AAP anti-obesogenic functions. Intestine-dwelling microbial population assessments discovered AAP to enhance (in a selective manner) Papillibacter cinnamivorans, a commensal bacterium having reduced presence within HFD mice. Notably, HFD mice treated with oral formulations of Papillibacter cinnamivorans diminished obesity and was linked to decreased intestinal lipid transportation. Datasets from the present study show that AAP thwarted dietary-driven obesity and metabolism-based disorders through regulating intestinal lipid transportation, a mechanism that is dependent on the gut commensal Papillibacter cinnamivorans. These results indicated AAP and Papillibacter cinnamivorans as newly identified pre- and probiotics that could possibly serve as novel countermeasure against obesity
2022-09-16 | MTBLS4469 | MetaboLights
Project description:Epidemiological studies highlight a strong association between obesity and colorectal cancer (CRC). This association appears stronger in men and a role for sex hormones is indicated by epidemiological studies. Especially estrogen is protective against CRC and correlated to several aspects of the metabolic syndrome. Anti-inflammatory and anti-tumorigenic effects of estrogen in colon have been demonstrated to act via estrogen receptor beta (ERβ). This led us to hypothesize that estrogenic signaling, through both systemic and local effects might modulate the colon microenvironment during HFD-induced obesity. In order to test our hypothesis mice were fed a control diet or a high fat diet (HFD) for 3 weeks and treated with different estrogenic ligands. In the present study, we demonstrate that there are sex-differences in the response to HFD-induced obesity and in the colon transcriptome. Both sexes develop obesity with an impaired circadian rhythm but the male metabolic profile is more sensitive to HFD and increased the colon epithelial cell proliferation. Females were resistant to impaired glucose metabolism, but HFD-feeding increased the infiltration of macrophages. Estrogen signaling in males, via ERα, presented anti-obesogenic effects. However, systemic and/or local activation of both ERα and ERβ restored the circadian rhythm in the males. In females, systemic activation of ERα restored the circadian rhythm, however, systemic and/or local activation of ERβ down-regulated the expression of macrophage markers. These results suggest that estrogen signaling through systemic and/or local activation of ERβ can regulate the colon microenvironment during HFD-induced obesity.
2020-10-07 | GSE149811 | GEO
Project description:Obesity and insulin resistance are associated with oxidative stress, which may be implicated in their progression. The kinase JNK1 emerged as a promising drug target for the treatment of obesity and type-2 diabetes. However, JNK1 is a key mediator of the oxidative stress response, promoting either cell dead or survival depending on magnitude and context of its activation. Furthermore, JNK inactivation shortens lifespan in drosophila and c. elegans. To learn on the safety and efficacy of long-term JNK inhibition in vertebrates, we investigated mice lacking JNK1 (JNK1-/-) exposed over a long period to an obesogenic high-fat diet (HFD). JNK1-/- mice chronically fed an HFD developed more skin oxidative damage because of reduced catalase expression, but also showed sustained protection from obesity, adipose tissue inflammation, steatosis, and insulin resistance, paralleled by decreased oxidative damage in fat and liver. We conclude that JNK1 is a relatively safe drug target for obesity-related diseases. RNA was collected from liver, skin and epididymal fat tissues from JNK1 KO mice and WT mice fed in high fat diet. Each condition was run in quadruplicate
2016-09-01 | E-GEOD-73759 | biostudies-arrayexpress
Project description:From a long time ago, supplementation of fermented enzyme foods could have worked health effects on the body in the east nevertheless, only a few studies reported functions of them such as weight loss and metabolic syndrome. Thus, it is necessary to be verified whether supplementation of fermented enzyme foods can act in the body as a functional material. Therefore, we investigated the anti-obesity effects of fermented mixed grain with digestive enzymes (FMG) in high-fat diet induced mice. Sixty C57BL/6J mice were divided into six dietary groups and fed a normal diet (ND), a high-fat diet (HFD), Bacilus Coagulans group, steamed grain group, low-dose fermented mixed grain group(L-FMG), high-dose fermented mixed grain group (H-FMG) supplement for 12 weeks. After sacrificing, body weight and body fat mass in H-FMG group were significantly decreased compared to HFD group with a simultaneous decrease in plasma lipids. Also, H-FMG significantly decreased the blood glucose and improved the glucose tolerance compared to HFD group. Moreover high-dose FMG supplementation dramatically decreased the levels of inflammatory cytokines which secreted from adipocyte. Taken together, our findings suggest that H-FMG ameliorate high fat-diet induced obesity and its complication and could be used as a potential preventive agent for obesity.
2020-09-12 | GSE157822 | GEO
Project description:Folic acid (FA) supplementation may protect from obesity and insulin resistance, the effects and mechanism of FA on chronic high-fat-diet-induced obesity-related metabolic disorders are not well elucidated. We adopted a genome-wide approach to directly examine whether FA supplementation affects the DNA methylation profile of mouse adipose tissue and identify the functional consequences of these changes. Mice were fed a high-fat diet (HFD), normal diet (ND) or an HFD supplemented with folic acid (20 μg/ml in drinking water) for 10 weeks, epididymal fat was harvested, and genome-wide DNA methylation analyses were performed using methylated DNA immunoprecipitation sequencing (MeDIP-seq). Mice exposed to the HFD expanded their adipose mass, which was accompanied by a significant increase in circulating glucose and insulin levels. FA supplementation reduced the fat mass and serum glucose levels and improved insulin resistance in HFD-fed mice. MeDIP-seq revealed distribution of differentially methylated regions (DMRs) throughout the adipocyte genome, with more hypermethylated regions in HFD mice. Methylome profiling identified DMRs associated with 3787 annotated genes from HFD mice in response to FA supplementation. Pathway analyses showed novel DNA methylation changes in adipose genes associated with insulin secretion, pancreatic secretion and type 2 diabetes. The differential DNA methylation corresponded to changes in the adipose tissue gene expression of Adcy3 and Rapgef4 in mice exposed to a diet containing FA. FA supplementation improved insulin resistance, decreased the fat mass, and induced DNA methylation and gene expression changes in genes associated with obesity and insulin secretion in obese mice fed a HFD.
2018-06-30 | GSE97576 | GEO
Project description:The High Fat Diet (HFD)-feeding significantly stimulated fat accumulation in Drosophila adults. Simultaneous feeding of known anti-obesity drugs that having the effect on rat and mouse, Quercetin Glycosides (QG) and Epigallocatechin gallate (EGCG) also suppressed fat accumulation in Drosophila at an equivalent concentration. Therefore, we have established a convenient model system to study on diet-induced fat accumulation and to evaluate effects of anti-obesity drugs using Drosophila. To understand overview of alterations of gene expression due to diet-induced fat accumulation and its suppression by the known anti-obesity drugs, we performed the RNA seq analyses. Consequently, mRNA levels of several genes involved in lipid metabolism, glycolysis/gluconeogenesis and anti-oxidative stress have changed in adults fed the HFD. Moreover, the levels altered in those fed on HFD supplemented with QG or EGCG. Our qRT-PCR further confirmed the RNA-seq data suggesting that expression of five genes essential for lipid metabolism was changed in HFD-fed animals and further altered in the animals treated with anti-obesity drugs. Among them, the most remarkable alteration was observed in dHSL gene encoding a lipase involved in lipid-storage after HFD feeding and the HFD supplemented with QG or EGCG. These changes are consistent with HFD-induced fat accumulation as well as the anti-obesity effects of those two drugs in mammals, suggesting that these genes play an important role in the anti-obesity effects of the drugs. These are the first evidences that whole profiles of altered gene expression under a condition of a diet-induced obesity and its suppression by anti-obesity drugs in Drosophila.
2018-10-20 | GSE121531 | GEO
Project description:Obesity has been shown to increase risk for cardiovascular disease and type-2 diabetes. In addition, it has been implicated in aggravation of neurological conditions such as Alzheimer’s. In the model organism Drosophila melanogaster, a physiological state mimicking diet-induced obesity can be induced by subjecting fruit flies to a solid medium disproportionately higher in sugar than protein (HSD) or that has been supplemented with a rich source of saturated fat (HFD). These flies can exhibit increased circulating glucose levels, increased triglyceride content, insulin-like peptide resistance, and behavior indicative of neurological decline, such as decreased climbing ability. We subjected Oregon-R-C flies to variants of the HSD, HFD, or normal (control) diet (ND), followed by a total RNA extraction from fly heads of each diet group for the purpose of Poly-A selected RNA-Sequencing. We targeted at least 50 million paired-end, stranded reads of 75 basepairs in size, and analyzed 4 biological replicates per dietary condition. Our objective was to identify the effects of obesogenic diets on transcriptome patterns, how they differed between obesogenic diets, and identify genes that may relate to pathogenesis accompanying an obesity-like state. Functional annotation and enrichment analysis among genes whose expression was significantly affected by the obesogenic diets indicated an overrepresentation of genes associated with immunity, metabolism, and hemocyanin in the HFD group, and CHK, cell cycle activity, and DNA binding and transcription in the HSD group. Heat map representation of genes affected by both diets illustrated a large fraction of differentially expressed genes between the two diet groups. Diets high in sugar and diets high in fat both have notableeffects on the Drosophila transcriptome in head tissue. The impacted genes, and how they may relate to pathogenesis in the Drosophila obesity-like state, warrant further experimental investigation. Our results also indicate differences in the effects of the HFD and HSD on expression profiles in head tissue of Oregon-R-C flies, despite the reportedly similar phenotypic impacts of the diets.
2017-09-28 | GSE104336 | GEO