{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T00:38:04Z","timestamp":1773794284391,"version":"3.50.1"},"reference-count":41,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,10,7]],"date-time":"2025-10-07T00:00:00Z","timestamp":1759795200000},"content-version":"vor","delay-in-days":279,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,1,1]],"date-time":"2025-01-01T00:00:00Z","timestamp":1735689600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["2021\/02401-9"],"award-info":[{"award-number":["2021\/02401-9"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["2022\/10682-0"],"award-info":[{"award-number":["2022\/10682-0"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","award":["2016\/15603-0"],"award-info":[{"award-number":["2016\/15603-0"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003593","name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico","doi-asserted-by":"publisher","award":["310699\/2022-3"],"award-info":[{"award-number":["310699\/2022-3"]}],"id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003593","name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico","doi-asserted-by":"publisher","award":["303095\/2021-0"],"award-info":[{"award-number":["303095\/2021-0"]}],"id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003593","name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico","doi-asserted-by":"publisher","award":["402687\/2021-3"],"award-info":[{"award-number":["402687\/2021-3"]}],"id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Diabetes Research"],"published-print":{"date-parts":[[2025,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      In individuals with Type 1 diabetes mellitus (T1D) who maintain good glycemic control and are free of chronic complications, lipid profiles are generally within normal ranges. However, impaired renal function or albuminuria alters this profile, contributing to the progression of diabetic kidney disease (DKD). This study hypothesized that, in urinary sediment cells from T1D individuals (\n                      <jats:italic>n<\/jats:italic>\n                      = 87), the mRNA expression of genes related to free fatty acid (FFA) uptake (\n                      <jats:italic>CD36<\/jats:italic>\n                      ,\n                      <jats:italic>FABP1<\/jats:italic>\n                      ,\n                      <jats:italic>SCL27A1<\/jats:italic>\n                      ,\n                      <jats:italic>SLC27A2<\/jats:italic>\n                      , and\n                      <jats:italic>SLC27A4<\/jats:italic>\n                      , which encode\n                      <jats:italic>FATP1<\/jats:italic>\n                      ,\n                      <jats:italic>FATP2<\/jats:italic>\n                      , and\n                      <jats:italic>FATP4<\/jats:italic>\n                      , respectively), albumin uptake (\n                      <jats:italic>LRP2<\/jats:italic>\n                      and\n                      <jats:italic>CUBN<\/jats:italic>\n                      ), inflammation (\n                      <jats:italic>IL1B<\/jats:italic>\n                      and\n                      <jats:italic>IL18<\/jats:italic>\n                      ), and fibrosis (\n                      <jats:italic>TGFB1<\/jats:italic>\n                      ) would vary depending on the degree of renal function decline and of urinary albumin excretion (UAE) and correlate with each other and with plasma lipid concentrations.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>CD36<\/jats:italic>\n                      expression was higher in urinary sediment cells of individuals with relevant renal function decline compared to those without relevant decline.\n                      <jats:italic>CD36<\/jats:italic>\n                      ,\n                      <jats:italic>IL1B<\/jats:italic>\n                      ,\n                      <jats:italic>TGFB1<\/jats:italic>\n                      , and\n                      <jats:italic>SLC27A4<\/jats:italic>\n                      (at the limit of statistical significance) expressions were higher in individuals with UAE &gt; 11\u2009mg\/g versus UAE \u2264 11\u2009mg\/g creatinine (cohort median value).\n                      <jats:italic>CD36<\/jats:italic>\n                      expression positively correlated with\n                      <jats:italic>IL1B<\/jats:italic>\n                      (\n                      <jats:italic>r<\/jats:italic>\n                      = 0.46) and\n                      <jats:italic>TGFB1<\/jats:italic>\n                      (\n                      <jats:italic>r<\/jats:italic>\n                      = 0.45) expressions, and\n                      <jats:italic>LRP2<\/jats:italic>\n                      expression positively correlated with\n                      <jats:italic>IL18<\/jats:italic>\n                      (\n                      <jats:italic>r<\/jats:italic>\n                      = 0.44) and\n                      <jats:italic>TGFB1<\/jats:italic>\n                      (\n                      <jats:italic>r<\/jats:italic>\n                      = 0.30). Expression of\n                      <jats:italic>SLC27A<\/jats:italic>\n                      genes also correlated with inflammatory and profibrotic genes. Plasma FFA concentrations positively correlated with\n                      <jats:italic>CD36<\/jats:italic>\n                      (\n                      <jats:italic>r<\/jats:italic>\n                      = 0.27) and\n                      <jats:italic>IL1B<\/jats:italic>\n                      (\n                      <jats:italic>r<\/jats:italic>\n                      = 0.30) expressions, while plasma triglyceride (TG) concentrations positively correlated with\n                      <jats:italic>CD36<\/jats:italic>\n                      (\n                      <jats:italic>r<\/jats:italic>\n                      = 0.22) and negatively correlated with\n                      <jats:italic>FABP1<\/jats:italic>\n                      (\n                      <jats:italic>r<\/jats:italic>\n                      = \u22120.28) expressions. Urinary sediment gene expression was modulated by statin (\n                      <jats:italic>IL18<\/jats:italic>\n                      ) and angiotensin II receptor blockers (\n                      <jats:italic>LRP2<\/jats:italic>\n                      ,\n                      <jats:italic>CUBN<\/jats:italic>\n                      , and\n                      <jats:italic>FABP1<\/jats:italic>\n                      ) use.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The expression of lipid metabolism\u2013related genes in urinary sediment cells, correlated with proinflammatory and profibrotic genes, as well as with plasma FFA and TG, and associated with clinical indicators of renal function, provides indirect evidence for the involvement of lipids in the pathogenesis of DKD.<\/jats:p>\n                  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