<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Choi YJ</submitter><funding>University of Michigan</funding><funding>NIDDK NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>JDRF</funding><funding>NIDDK</funding><funding>Boettcher Foundation and Intramural Research Program at NIDDK and CDC</funding><pagination>e183984</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11645151</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>134(24)</volume><pubmed_abstract>BACKGROUNDIn type 1 diabetes (T1D), impaired insulin sensitivity may contribute to the development of diabetic kidney disease (DKD) through alterations in kidney oxidative metabolism.METHODSYoung adults with T1D (n = 30) and healthy controls (HCs) (n = 20) underwent hyperinsulinemic-euglycemic clamp studies, MRI, 11C-acetate PET, kidney biopsies, single-cell RNA-Seq, and spatial metabolomics to assess this relationship.RESULTSParticipants with T1D had significantly higher glomerular basement membrane (GBM) thickness compared with HCs. T1D participants exhibited lower insulin sensitivity and cortical oxidative metabolism, correlating with higher insulin sensitivity. Proximal tubular transcripts of TCA cycle and oxidative phosphorylation enzymes were lower in T1D. Spatial metabolomics showed</pubmed_abstract><journal>The Journal of clinical investigation</journal><pubmed_title>Attenuated kidney oxidative metabolism in young adults with type 1 diabetes.</pubmed_title><pmcid>PMC11645151</pmcid><funding_grant_id>2-SRA-2019-845-S-B</funding_grant_id><funding_grant_id>P30 DK116073</funding_grant_id><funding_grant_id>L40 HL159798</funding_grant_id><funding_grant_id>R01 DK129211</funding_grant_id><funding_grant_id>P30 DK020572</funding_grant_id><funding_grant_id>R01 HL165433</funding_grant_id><funding_grant_id>21FED2100157DPG</funding_grant_id><funding_grant_id>P30 DK081943</funding_grant_id><funding_grant_id>K23 HL159292</funding_grant_id><funding_grant_id>R01 DK137844</funding_grant_id><funding_grant_id>R01 DK132399</funding_grant_id><funding_grant_id>K23 DK125529</funding_grant_id><funding_grant_id>K08 DK124449</funding_grant_id><pubmed_authors>Zhang G</pubmed_authors><pubmed_authors>Brosius FC</pubmed_authors><pubmed_authors>Tamayo IM</pubmed_authors><pubmed_authors>Puelles VG</pubmed_authors><pubmed_authors>Goodrich JA</pubmed_authors><pubmed_authors>Alakwaa F</pubmed_authors><pubmed_authors>Chin BB</pubmed_authors><pubmed_authors>Kendrick J</pubmed_authors><pubmed_authors>Demeke DS</pubmed_authors><pubmed_authors>Prasad P</pubmed_authors><pubmed_authors>Gurung BK</pubmed_authors><pubmed_authors>Nair V</pubmed_authors><pubmed_authors>MacDonald A</pubmed_authors><pubmed_authors>Saulnier PJ</pubmed_authors><pubmed_authors>Schaub JA</pubmed_authors><pubmed_authors>Pyle L</pubmed_authors><pubmed_authors>Street K</pubmed_authors><pubmed_authors>Cherney DZ</pubmed_authors><pubmed_authors>de Boer IH</pubmed_authors><pubmed_authors>Naik AS</pubmed_authors><pubmed_authors>Flynn M</pubmed_authors><pubmed_authors>Venkatachalam MA</pubmed_authors><pubmed_authors>Shah VN</pubmed_authors><pubmed_authors>Gross S</pubmed_authors><pubmed_authors>van Raalte DH</pubmed_authors><pubmed_authors>Nelson RG</pubmed_authors><pubmed_authors>Snell-Bergeon JK</pubmed_authors><pubmed_authors>Hodgin JB</pubmed_authors><pubmed_authors>Otto EA</pubmed_authors><pubmed_authors>Richard G</pubmed_authors><pubmed_authors>Sharma K</pubmed_authors><pubmed_authors>Blondin DP</pubmed_authors><pubmed_authors>Tommerdahl K</pubmed_authors><pubmed_authors>Driscoll L</pubmed_authors><pubmed_authors>Yang Y</pubmed_authors><pubmed_authors>Ladd P</pubmed_authors><pubmed_authors>McCown PJ</pubmed_authors><pubmed_authors>Kretzler M</pubmed_authors><pubmed_authors>Nadeau KJ</pubmed_authors><pubmed_authors>Choi YJ</pubmed_authors><pubmed_authors>Li LP</pubmed_authors><pubmed_authors>Ruiz A</pubmed_authors><pubmed_authors>Narongkiatikhun P</pubmed_authors><pubmed_authors>Bjornstad P</pubmed_authors><pubmed_authors>Birznieks C</pubmed_authors><pubmed_authors>Vigers T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Attenuated kidney oxidative metabolism in young adults with type 1 diabetes.</name><description>BACKGROUNDIn type 1 diabetes (T1D), impaired insulin sensitivity may contribute to the development of diabetic kidney disease (DKD) through alterations in kidney oxidative metabolism.METHODSYoung adults with T1D (n = 30) and healthy controls (HCs) (n = 20) underwent hyperinsulinemic-euglycemic clamp studies, MRI, 11C-acetate PET, kidney biopsies, single-cell RNA-Seq, and spatial metabolomics to assess this relationship.RESULTSParticipants with T1D had significantly higher glomerular basement membrane (GBM) thickness compared with HCs. T1D participants exhibited lower insulin sensitivity and cortical oxidative metabolism, correlating with higher insulin sensitivity. Proximal tubular transcripts of TCA cycle and oxidative phosphorylation enzymes were lower in T1D. Spatial metabolomics showed</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2026-06-03T03:08:03.816Z</modification><creation>2025-04-04T01:54:29.228Z</creation></dates><accession>S-EPMC11645151</accession><cross_references><pubmed>39436695</pubmed><doi>10.1172/JCI183984</doi></cross_references></HashMap>