{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T02:42:37Z","timestamp":1772160157772,"version":"3.50.1"},"reference-count":39,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2025,3,5]],"date-time":"2025-03-05T00:00:00Z","timestamp":1741132800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100004339","name":"Sanofi","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004339","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["dom-pubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2025,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Postprandial hyperlipidaemia (PPL), characterized by elevated triglyceride (TG) concentrations after a meal, is common in type 2 diabetes (T2D) and is often recognized as an independent cardiovascular risk factor. Here, we aimed to assess the effect of proprotein convertase subtilisin\/kexin type 9 (PCSK9) inhibition by alirocumab on PPL in patients with T2D.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>\n                      EUTERPE is a randomized, double\u2010blind, placebo\u2010controlled cross\u2010over trial conducted in male patients with T2D. Participants received sequentially two sequences of 10\u2010week treatment (alirocumab 75\u2009mg Q2W or placebo s\/c) with a wash\u2010out period of 10\u2009weeks. The primary end\u2010point was the percentage reduction in plasma TG response after an oral fat load (incremental area under the curve [iAUC]\n                      <jats:sub>0\u20108h<\/jats:sub>\n                      TG). Secondary end\u2010points included mass spectrometry\u2010based apolipoprotein measurements and nuclear magnetic resonance (NMR)\u2010based lipoprotein profiling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Fourteen participants were included: age 59\u2009\u00b1\u20099\u2009years, BMI 32.8\u2009\u00b1\u20095.5\u2009kg\/m\n                      <jats:sup>2<\/jats:sup>\n                      , HbA\n                      <jats:sub>1C<\/jats:sub>\n                      6.7\u2009\u00b1\u20090.5%. Compared to placebo, alirocumab did not reduce PPL (iAUC\n                      <jats:sub>0\u20108h<\/jats:sub>\n                      TG: \u20105% [CI 95%: \u221228, +25],\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.68). Alirocumab decreased fasting non\u2010HDL cholesterol (\u221238.5\u2009\u00b1\u20095.6%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0003), remnant cholesterol (\u221220.0\u2009\u00b1\u200913.3%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.04), apoB100 (\u221221.2\u2009\u00b1\u20096.4%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.004) and apoE (\u221215.3\u2009\u00b1\u20096.6%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.02) concentrations. NMR analyses showed that alirocumab decreased both postprandial VLDL\n                      <jats:sub>2<\/jats:sub>\n                      cholesterol (\u221242% [\u221255, \u221225],\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001) and IDL cholesterol (\u221226% [\u221238, \u221212],\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0007), without effect on VLDL\n                      <jats:sub>1<\/jats:sub>\n                      cholesterol or TG concentrations.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Inhibition of PCSK9 by alirocumab did not reduce PPL in T2D, confirming that PCSK9 controls remnant cholesterol catabolism rather than intestinal chylomicron production.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/dom.16305","type":"journal-article","created":{"date-parts":[[2025,3,11]],"date-time":"2025-03-11T17:19:04Z","timestamp":1741713544000},"page":"3006-3016","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Effect of alirocumab on postprandial hyperlipidaemia in patients with type 2 diabetes: A randomized, double\u2010blind, placebo\u2010controlled, cross\u2010over trial"],"prefix":"10.1111","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1580-8040","authenticated-orcid":false,"given":"Bertrand","family":"Cariou","sequence":"first","affiliation":[{"name":"Nantes Universit\u00e9, CHU Nantes, CNRS, Inserm l'institut du thorax  Nantes France"},{"name":"CHU Nantes, Inserm, CIC1413 l'institut du thorax  Nantes France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6838-312X","authenticated-orcid":false,"given":"An","family":"Thys","sequence":"additional","affiliation":[{"name":"Nantes Universit\u00e9, CHU Nantes, CNRS, Inserm l'institut du thorax  Nantes France"},{"name":"CHU Nantes, Inserm, CIC1413 l'institut du thorax  Nantes France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ars\u00eanio Rodrigues","family":"Oliveira","sequence":"additional","affiliation":[{"name":"Nantes Universit\u00e9, CHU Nantes, CNRS, Inserm l'institut du thorax  Nantes France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marine P. 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