{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Christie HE"],"funding":["National Institute of Diabetes and Digestive and Kidney Diseases"],"pagination":["e200913"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12948432"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["136(5)"],"pubmed_abstract":["BACKGROUNDAmino acid (AA) concentrations are increased in prediabetes and diabetes. Since AAs stimulate glucagon secretion, which should then increase hepatic AA catabolism, it has been hypothesized that hepatic resistance (associated with hepatic fat content) to glucagon's actions on AA metabolism leads to hyperglucagonemia and hyperglycemia.METHODSTo test this hypothesis, we therefore studied lean and obese individuals, the latter group with and without hepatic steatosis as defined by proton density fat fraction (PDFF) > 5%. After an overnight fast, femoral vein, femoral artery, and hepatic vein catheters were placed. [3-3H] glucose and l-[1-13C,15N]-leucine were used to measure glucose turnover and leucine oxidation, respectively. During a hyperglycemic clamp, an AA mixture was infused "],"journal":["The Journal of clinical investigation"],"pubmed_title":["Hepatic steatosis in humans is associated with preserved glucagon action on amino acid metabolism."],"pmcid":["PMC12948432"],"funding_grant_id":["DK116231,DK78646,DK126206"],"pubmed_authors":["Nair KS","Jensen MD","Bailey KR","Vella A","Egan AM","Fleming CJ","Boscolo F","Jundt M","Dalla Man C","Thompson SM","Mohan S","Andrews JC","Christie HE"],"additional_accession":[]},"is_claimable":false,"name":"Hepatic steatosis in humans is associated with preserved glucagon action on amino acid metabolism.","description":"BACKGROUNDAmino acid (AA) concentrations are increased in prediabetes and diabetes. Since AAs stimulate glucagon secretion, which should then increase hepatic AA catabolism, it has been hypothesized that hepatic resistance (associated with hepatic fat content) to glucagon's actions on AA metabolism leads to hyperglucagonemia and hyperglycemia.METHODSTo test this hypothesis, we therefore studied lean and obese individuals, the latter group with and without hepatic steatosis as defined by proton density fat fraction (PDFF) > 5%. After an overnight fast, femoral vein, femoral artery, and hepatic vein catheters were placed. [3-3H] glucose and l-[1-13C,15N]-leucine were used to measure glucose turnover and leucine oxidation, respectively. During a hyperglycemic clamp, an AA mixture was infused ","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Mar","modification":"2026-07-17T01:09:04.061Z","creation":"2026-07-12T03:12:43.352Z"},"accession":"S-EPMC12948432","cross_references":{"pubmed":["41433112"],"doi":["10.1172/JCI200913"]}}