{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE301nnn/GSE301098/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE301098"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Gene expression analysis in hepatocytes in response to hepatocyte-specific Succinate Receptor 1 (SUCNR1) deletion","description":"The liver plays a crucial role in metabolic adaptations in response to nutrients, a function that is critically dependent on its zonated structure. Succinate, a key intermediate of the tricarboxylic acid cycle, has emerged as a postprandial signaling metabolite that regulates metabolic adaptations to food intake in adipose tissue and pancreatic beta cells through its receptor SUCNR1. Considering that SUCNR1 is also expressed in hepatocytes, we hypothesized a role for the succinate-SUCNR1 axis in liver metabolic homeostasis. To better understand the role of Sucnr1in hepatocytes, we generated a mouse model specifically lacking Sucnr1 in hepatocytes (Hep-Sucnr1 KO mice) and performed an RNA-seq of isolated hepatocytes from controls (Sucnr1 fl/fl mice) and Hep-Sucnr1 KO mice.","dates":{"publication":"2026/04/28"},"accession":"GSE301098","cross_references":{"GSM":["GSM9075393","GSM9075398","GSM9075394","GSM9075395","GSM9075396","GSM9075397"],"GPL":["24247"],"GSE":["301098"],"taxon":["Mus musculus"]}}