{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Yiew NKH"],"funding":["NIDDK NIH HHS","NIEHS NIH HHS","NHLBI NIH HHS"],"pubmed_abstract":["The liver coordinates the systemic response to nutrient deprivation and availability by producing glucose from gluconeogenesis during fasting and synthesizing lipids via <i>de novo</i> lipogenesis (DNL) when carbohydrates are abundant. Mitochondrial pyruvate metabolism is thought to play important roles in both gluconeogenesis and DNL. We examined the effects of hepatocyte-specific mitochondrial pyruvate carrier (MPC) deletion on the fasting-refeeding response. Rates of DNL during refeeding were impaired by liver MPC deletion, but this did not reduce intrahepatic lipid content. During fasting, glycerol is converted to glucose by two pathways; a direct cytosolic pathway essentially reversing glycolysis and an indirect mitochondrial pathway requiring the MPC. MPC deletion reduced the incorporation of <sup>13</sup>C-glycerol into TCA cycle metabolites but not into newly synthesized glucose. However, suppression of glycerol metabolism did not affect glucose concentrations in fasted hepatocyte-specific MPC-deficient mice. Thus, glucose production by kidney and intestine may compensate for MPC deficiency in hepatocytes."],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2023.02.17.528992"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9949129"],"repository":["biostudies-literature"],"pubmed_title":["Effects of hepatic mitochondrial pyruvate carrier deficiency on de novo lipogenesis and glycerol-mediated gluconeogenesis in mice."],"pmcid":["PMC9949129"],"funding_grant_id":["K01 DK137050","R35 ES028365","T32 DK007120","T32 HL134635","R01 DK117657","P30 DK020579","P30 DK052574","K01 DK133630","P30 DK056341","R01 DK128168","K01 DK126990","P30 DK127984","R01 DK104735"],"pubmed_authors":["Yiew NKH","Finck BN","Deja S","Fu X","Jarasvaraparn C","Burgess SC","Cho K","Patti GJ","Jacome-Sosa M","Singer JM","Ferguson D","Mukherjee S","Lutkewitte AJ"],"additional_accession":[]},"is_claimable":false,"name":"Effects of hepatic mitochondrial pyruvate carrier deficiency on de novo lipogenesis and glycerol-mediated gluconeogenesis in mice.","description":"The liver coordinates the systemic response to nutrient deprivation and availability by producing glucose from gluconeogenesis during fasting and synthesizing lipids via <i>de novo</i> lipogenesis (DNL) when carbohydrates are abundant. Mitochondrial pyruvate metabolism is thought to play important roles in both gluconeogenesis and DNL. We examined the effects of hepatocyte-specific mitochondrial pyruvate carrier (MPC) deletion on the fasting-refeeding response. Rates of DNL during refeeding were impaired by liver MPC deletion, but this did not reduce intrahepatic lipid content. During fasting, glycerol is converted to glucose by two pathways; a direct cytosolic pathway essentially reversing glycolysis and an indirect mitochondrial pathway requiring the MPC. MPC deletion reduced the incorporation of <sup>13</sup>C-glycerol into TCA cycle metabolites but not into newly synthesized glucose. However, suppression of glycerol metabolism did not affect glucose concentrations in fasted hepatocyte-specific MPC-deficient mice. Thus, glucose production by kidney and intestine may compensate for MPC deficiency in hepatocytes.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Aug","modification":"2026-05-06T03:12:56.955Z","creation":"2025-04-06T08:48:32.992Z"},"accession":"S-EPMC9949129","cross_references":{"pubmed":["36824879"],"doi":["10.1101/2023.02.17.528992"]}}