Ask about this productRelated genes to: PPARA antibody
- Gene:
- PPARA NIH gene
- Name:
- peroxisome proliferator activated receptor alpha
- Previous symbol:
- PPAR
- Synonyms:
- hPPAR, NR1C1
- Chromosome:
- 22q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-01
- Date modifiied:
- 2016-10-05
Related products to: PPARA antibody
Related articles to: PPARA antibody
- The health benefits of tomato consumption may derive from bioactive compounds other than lycopene in tomatoes. 15-Cis-phytoene, a colorless precursor of lycopene abundant in tomatoes, has not been well studied for its biological activity. We investigated whether dietary 15-cis-phytoene protects against metabolic dysfunction-associated steatotic liver disease (MASLD) and whether this protection depends on the carotenoid cleavage enzymes, beta-carotene-15,15'-oxygenase 1 (BCO1) and beta-carotene-9',10'-oxygenase (BCO2). Wild-type (WT) and BCO1/BCO2 double knock-out (DKO) mice were fed a high-refined carbohydrate diet (HRCD) with or without 15-cis-phytoene supplementation for 24 weeks. 15-Cis-phytoene supplementation markedly increased 15-cis and all-trans phytoene concentrations in intestine, liver, and serum, and significantly attenuated HRCD-induced MASLD in WT mice. The protective effects of phytoene on MASLD in WT mice were associated with increased hepatic mRNA and protein levels of SIRT1, PGC1α, and PPARα; enhanced AMPK and ACC phosphorylation; and upregulated fatty acid oxidation genes, but not with the gut microbiota composition. Despite much higher phytoene accumulation in the liver and serum, phytoene did not exhibit protection against HRCD-induced MASLD in DKO mice. Phytoene is a biologically active compound that contributes to the benefits of tomato consumption against MASLD. Its protective effects are likely mediated by cleavage metabolites through BCO1/BCO2. - Source: PubMed
Lee Na YounLee JenniferMatthan Nirupa RLamon-Fava StefaniaWang Xiang-Dong - Diabetic osteoporosis (DO) is a chronic consequence of diabetes mellitus marked by disrupted bone metabolism and elevated fracture risk, with no effective strategies currently available. Betulinic acid (BA) is a natural pentacyclic triterpenoid demonstrating anti-diabetic, anti-inflammatory, and osteoprotective effects. This research aimed to clarify the molecular mechanisms of BA in DO using network pharmacology, molecular docking, and molecular dynamics simulations. - Source: PubMed
Publication date: 2026/08/06
Sharma SheenamChaudhary RishabhSharma ChiragDabral SwarnaBansal SeemaSharma NeelamGupta Sumeet - Adipocyte depots throughout the body are physiologically and molecularly distinct. With age, adipocytes increase in and around aged thymi. Yet thymic adipocytes lack molecular characterization. We developed methods to isolate adipocyte nuclei from mouse thymi. Single-nucleus multi-omic analysis of male and female mice aged 4-9 months reveals that thymic adipocytes are heterogeneous, with two distinct populations. One subpopulation harbors a transcription and chromatin signature consistent with beige fat. Another subpopulation resembles classic white adipose tissue and expresses genes associated with epithelial-to-mesenchymal transition (EMT). Analysis of differentially open chromatin identifies binding sites for Foxn1 and HIF-1α/Arnt in the white adipose population, consistent with a thymic epithelial and/or hypoxic origin for these cells. Immunofluorescence confirmed the expression of UCP1 protein in cells in subcapsular cortical regions of the thymic parenchyma. This resource reveals a complex milieu of thymic adipocytes and identifies multiple avenues for probing their ontogeny, dynamics, and functional significance. - Source: PubMed
Publication date: 2026/08/11
Schwakopf JoonSyage Amber RFranzini AncaVarley Katherine ETantin Dean - Agonists of the lipid-sensing PPAR nuclear receptors, including PPARα, are being explored as therapies for metabolic disorders due to their roles in metabolic and anti-inflammatory processes. PPARα transcriptional programs have tissue-dependent features, yet there is a lack of genetic tools to study tissue-specific signaling activation without the addition of a systemic agonist. We aimed to investigate intestinal epithelial cell (IEC)-specific roles of PPARα signaling using a novel transgenic mouse that enables spatial and temporal control of Ppara overexpression. CAG-Ppara, -EGFP mice were bred to Villin-CreERT2 to establish the IEC-Ppara mouse, which was compared to littermate controls 2 weeks after tamoxifen exposure. IEC-Ppara mice had increased Ppara mRNA and PPARα protein in the intestinal epithelium. Transcriptional analysis of intestinal tissue from IEC-Ppara mice showed upregulation of PPARα target genes and functional enrichment for fatty acid catabolic processes. As expected, the enterocytes of IEC-Ppara mice were primed to absorb lipids following oral administration of an olive oil bolus. Unexpectedly, the enteroendocrine hormone Gip was among the most downregulated genes. GIP-positive cells were reduced in the intestines of IEC-Ppara mice and in mice treated with PPARα agonist WY-14643. Circulating GIP hormone, but not GLP-1 hormone, was reduced in IEC-Ppara mice. GLP-1-positive cells and hormone were unchanged. Consistent with reduced GIP function, IEC-Ppara mice consumed more food. These findings reveal PPARα as a regulator of GIP and support a new framework in which PPARα signaling influences systemic energy balance via a gut hormone axis. This study could have future impact on understanding responses to therapies targeting PPAR or incretin signaling. - Source: PubMed
Publication date: 2026/08/13
Socha Jacob JPavithran SwathiBurger Courtney AKarns RebekahLee Avelina WLang RichardMoreno-Fernandez Maria EStandage Stephen WVanDussen Kelli L - This study explored the genetic evidence linking triglyceride-related pathways and lipid-lowering drug targets with endometriosis risk and investigated the genetic association between TG levels and EM. Using genome-wide association study (GWAS) data, a two-sample Mendelian randomization (MR) analysis was conducted, estimating the association between genetically predicted TG levels and EM risk (OR = 1.1853, 95% CI: 1.070-1.313, p = 0.0011). Seven TG-lowering drug target genes (SLC9A1, SCN3A, VEGFA, APOA1, TNF, ITGAV, BACE1) were identified. Transcriptome analysis revealed that SCN3A, BACE1, and APOA1 were significantly upregulated in EM patients compared to healthy controls. Enrichment pathway analysis showed that these genes are involved in lipid transport, localization, cell adhesion, and blood vessel development. PPARA was predicted to act as a transcription factor for five of these genes, while estrogen receptor 1 (ESR1) was predicted to regulate the majority of the others. Among the TG inhibitors examined, fibrate-related targets showed relatively broader target coverage in the present genetic analyses. These findings suggest that TG-related pathways and lipid-lowering drug targets, particularly fibrate-related targets, may be relevant to EM biology and warrant further experimental and clinical validation. - Source: PubMed
Publication date: 2026/08/13
Li YonghongHe JiananZhang YuanqingYang MinJia ZhimaoFan YidanLiu ShuyunQi Mengsha