{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li J"],"funding":["Novo Nordisk Fonden (Novo Nordisk Foundation)","U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging)","U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases)","U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI)","American Heart Association (American Heart Association, Inc.)"],"pagination":["660-670"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12920144"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["32(2)"],"pubmed_abstract":["The human metabolome reflects complex metabolic states affected by genetic and environmental factors. However, metabolites associated with type 2 diabetes (T2D) risk and their determinants remain insufficiently characterized. Here we integrated blood metabolomic, genomic and lifestyle data from up to 23,634 initially T2D-free participants from ten cohorts. Of 469 metabolites examined, 235 were associated with incident T2D during up to 26 years of follow-up, including 67 associations not previously reported across bile acid, lipid, carnitine, urea cycle and arginine/proline, glycine and histidine pathways. Further genetic analyses linked these metabolites to signaling pathways and clinical traits central to T2D pathophysiology, including insulin resistance, glucose/insulin response, ectopic"],"journal":["Nature medicine"],"pubmed_title":["Circulating metabolites, genetics and lifestyle factors in relation to future risk of type 2 diabetes."],"pmcid":["PMC12920144"],"funding_grant_id":["R01AG085320","R01HL060712","U01DK140761","R01DK119268; R01DK126698; U01DK140761; R01DK120870","R01HL136266","R00DK122128","R01HL153178","23POST1020455","R01DK081572","NNF24OC0095435","R01DK134672","K24HL152440","R01HL060712; R01HL170904"],"pubmed_authors":["Gerszten RE","Dupuis J","Florez JC","Rotter JI","Guo X","Merino J","Boerwinkle E","Rich SS","Alkis T","Truong B","Wang TJ","Rebholz CM","Bhupathiraju SN","Liang L","Wang X","Yao J","Li J","Manson JE","Hu FB","Wood AC","Salas-Salvado J","Rexrode KM","Porneala BC","Liu CT","Hu J","Brody JA","Martinez-Gonzalez MA","Kaplan RC","Yun H","Jia C","Mei Z","Meigs JB","Han X","Clish CB","Liu S","Tucker KL","Sotoodehnia N","Qi Q","Liu Y","Jung SY","Selvin E","Lemaitre RN","Guasch-Ferre M","Tinker LF","Ruiz-Canela M","Eliassen AH","Luo K","Yu B","Zhang X","Moon EH","Liu G","North KE"],"additional_accession":[]},"is_claimable":false,"name":"Circulating metabolites, genetics and lifestyle factors in relation to future risk of type 2 diabetes.","description":"The human metabolome reflects complex metabolic states affected by genetic and environmental factors. However, metabolites associated with type 2 diabetes (T2D) risk and their determinants remain insufficiently characterized. Here we integrated blood metabolomic, genomic and lifestyle data from up to 23,634 initially T2D-free participants from ten cohorts. Of 469 metabolites examined, 235 were associated with incident T2D during up to 26 years of follow-up, including 67 associations not previously reported across bile acid, lipid, carnitine, urea cycle and arginine/proline, glycine and histidine pathways. Further genetic analyses linked these metabolites to signaling pathways and clinical traits central to T2D pathophysiology, including insulin resistance, glucose/insulin response, ectopic","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Feb","modification":"2026-07-16T12:59:48.81Z","creation":"2026-07-09T10:57:03.675Z"},"accession":"S-EPMC12920144","cross_references":{"pubmed":["41535386"],"doi":["10.1038/s41591-025-04105-8"]}}