2023
1569-P: Lysophosphatidic Acid Mediates Inflammation in Liver and White Adipose Tissue in a Rat Model of 1-acyl-sn-glycerol-3-phosphate Acyltransferase 2 Deficiency
SAKUMA I, GASPAR R, LUUKKONEN P, KAHN M, MURRAY S, SAMUEL V, PETERSEN K, SHULMAN G. 1569-P: Lysophosphatidic Acid Mediates Inflammation in Liver and White Adipose Tissue in a Rat Model of 1-acyl-sn-glycerol-3-phosphate Acyltransferase 2 Deficiency. Diabetes 2023, 72 DOI: 10.2337/db23-1569-p.Peer-Reviewed Original ResearchWhite adipose tissueControlled-release mitochondrial protonophoreCongenital generalized lipodystrophyAGPAT2 deficiencyHepatic inflammationASO treatmentAdipose tissueLysophosphatidic acidAdult male SD ratsAntisense oligonucleotideMale SD ratsNovel therapeutic targetNovo NordiskCRMP treatmentFortress BiotechWAT inflammationDohme Corp.SD ratsRat modelAGPAT2 geneGeneralized lipodystrophyInflammationTherapeutic targetIonis PharmaceuticalsDeficient animals1558-P: The Mitochondrial Calcium Uniporter Regulates Hepatic Mitochondrial Oxidation and Intracellular Redox In Vivo
LAMOIA T, HUBBARD B, GUERRA M, GOODMAN R, NATHANSON M, SHULMAN G. 1558-P: The Mitochondrial Calcium Uniporter Regulates Hepatic Mitochondrial Oxidation and Intracellular Redox In Vivo. Diabetes 2023, 72 DOI: 10.2337/db23-1558-p.Peer-Reviewed Original ResearchNonalcoholic fatty liver diseaseHepatic mitochondrial oxidationMitochondrial calcium uniporterHepatocellular redox stateFatty liver diseaseEctopic lipid accumulationType 2 diabetesHepatic lipid contentNovel therapeutic targetMitochondrial oxidationHepatic triacylglycerol contentMitochondrial calcium influxMitochondrial redox ratioMitochondrial calciumKnockout mouse modelFortress BiotechMitochondrial fat oxidationNonalcoholic steatohepatitisLiver diseaseWT miceKO miceMetabolic dysfunctionCalcium uniporterCalcium influxMouse model
2020
MON-635 FDXR Regulates Iron Metabolism and Glucose Metabolism in Liver
Sakuma I, Yokoyama M, Yamagata K, Hashimoto N, Nakayama A, Shulman G, Tanaka T. MON-635 FDXR Regulates Iron Metabolism and Glucose Metabolism in Liver. Journal Of The Endocrine Society 2020, 4: mon-635. PMCID: PMC7207756, DOI: 10.1210/jendso/bvaa046.1557.Peer-Reviewed Original ResearchNon-alcoholic fatty liver diseaseForkhead box protein O1Iron metabolismFoxO1 nuclear exclusionOxidative stressFatty liver diseaseSerum ferritin levelsMouse liverHigh-fat dietType 2 diabetesPathogenesis of diabetesNovel therapeutic targetIron regulatory genesHepatic iron contentTreatment of diabetesHepG2 cellsBox protein O1Glucose intoleranceMost patientsFerritin levelsLiver diseaseClinical studiesGluconeogenesis activationFDXR expressionGlucose metabolism
2008
N-acylphosphatidylethanolamine, a Gut- Derived Circulating Factor Induced by Fat Ingestion, Inhibits Food Intake
Gillum MP, Zhang D, Zhang XM, Erion DM, Jamison RA, Choi C, Dong J, Shanabrough M, Duenas HR, Frederick DW, Hsiao JJ, Horvath TL, Lo CM, Tso P, Cline GW, Shulman GI. N-acylphosphatidylethanolamine, a Gut- Derived Circulating Factor Induced by Fat Ingestion, Inhibits Food Intake. Cell 2008, 135: 813-824. PMID: 19041747, PMCID: PMC2643061, DOI: 10.1016/j.cell.2008.10.043.Peer-Reviewed Original ResearchConceptsFood intakeInhibits food intakeTreatment of obesityNovel therapeutic targetCentral nervous systemUnknown physiological significanceFat ingestionCirculating factorsN-acylphosphatidylethanolaminePlasma lipidsIntracerebroventricular infusionPhysiologic dosesSystemic administrationTherapeutic targetBody weightNervous systemIngested fatSmall intestineIntakeTaste aversionInfusionPhysiological significanceNanomolar amountsObesityHypothalamus