<HashMap><database>GEO</database><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE295094</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Transcriptomic profiling of hepatic response to glucose intake during fasting and feeding states in a mouse model of metabolic dysfunction</name><description>The global increase in metabolic dysfunction-associated steatotic liver disease (MASLD) is linked to high sugar intake, especially in Western diets. However, how glucose consumption during fasting versus feeding states affects hepatic fat synthesis and insulin signaling remains unclear. In this study, we applied an every-other-day fasting (EODF) protocol in mice and divided them into three groups: a control group, a feeding-glucose group (glucose water during feeding), and a fasting-glucose group (glucose water during fasting). We measured liver triglyceride content, insulin sensitivity, and expression of hepatic lipogenic genes. Our findings reveal that glucose intake during feeding promotes hepatic fat accumulation, while glucose intake during fasting impairs insulin signaling in the liver.</description><dates><publication>2026/05/31</publication></dates><accession>GSE295094</accession><cross_references><GSM>GSM8942262</GSM><GSM>GSM8942263</GSM><GSM>GSM8942261</GSM><GSM>GSM8942268</GSM><GSM>GSM8942266</GSM><GSM>GSM8942267</GSM><GSM>GSM8942264</GSM><GSM>GSM8942265</GSM><GPL>24247</GPL><GSE>295094</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>