{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T13:39:18Z","timestamp":1791812358821,"version":"4.3.4"},"reference-count":38,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","license":[{"start":{"date-parts":[[2022,5,15]],"date-time":"2022-05-15T00:00:00Z","timestamp":1652572800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/ http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100016022","name":"Data Center of Management Science, National Natural Science Foundation of China - Peking University","doi-asserted-by":"publisher","award":["82070474"],"award-info":[{"award-number":["82070474"]}],"id":[{"id":"10.13039\/501100016022","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background and Aims<\/jats:title>\n                    <jats:p>Peroxisome proliferator\u2010activated receptor \u03b1 (PPAR\u03b1) regulates fatty acid transport and catabolism in liver. However, the role of intestinal PPAR\u03b1 in lipid homeostasis is largely unknown. Here, intestinal PPAR\u03b1 was examined for its modulation of obesity and NASH.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Approach and Results<\/jats:title>\n                    <jats:p>\n                      Intestinal PPAR\u03b1 was activated and fatty acid\u2010binding protein 1 (FABP1) up\u2010regulated in humans with obesity and high\u2010fat diet (HFD)\u2013fed mice as revealed by using human intestine specimens or HFD\/high\u2010fat, high\u2010cholesterol, and high\u2010fructose diet (HFCFD)\u2010fed C57BL\/6N mice and\n                      <jats:italic toggle=\"yes\">PPARA<\/jats:italic>\n                      \u2010humanized, peroxisome proliferator response element\u2013luciferase mice. Intestine\u2010specific\n                      <jats:italic toggle=\"yes\">Ppara<\/jats:italic>\n                      or\n                      <jats:italic toggle=\"yes\">Fabp1<\/jats:italic>\n                      disruption in mice fed a HFD or HFCFD decreased obesity\u2010associated metabolic disorders and NASH. Molecular analyses by luciferase reporter assays and chromatin immunoprecipitation assays in combination with fatty acid uptake assays in primary intestinal organoids revealed that intestinal PPAR\u03b1 induced the expression of FABP1 that in turn mediated the effects of intestinal PPAR\u03b1 in modulating fatty acid uptake. The PPAR\u03b1 antagonist GW6471 improved obesity and NASH, dependent on intestinal PPAR\u03b1 or FABP1. Double\u2010knockout (\n                      <jats:italic toggle=\"yes\">Ppara\/Fabp1<\/jats:italic>\n                      <jats:sup>\u0394IE<\/jats:sup>\n                      ) mice demonstrated that intestinal\n                      <jats:italic toggle=\"yes\">Ppara<\/jats:italic>\n                      disruption failed to further decrease obesity and NASH in the absence of intestinal FABP1. Translationally, GW6471 reduced human PPARA\u2010driven intestinal fatty acid uptake and improved obesity\u2010related metabolic dysfunctions in\n                      <jats:italic toggle=\"yes\">PPARA<\/jats:italic>\n                      \u2010humanized, but not\n                      <jats:italic toggle=\"yes\">Ppara<\/jats:italic>\n                      \u2010null, mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Intestinal PPAR\u03b1 signaling promotes NASH progression through regulating dietary fatty acid uptake through modulation of FABP1, which provides a compelling therapeutic target for NASH treatment.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/hep.32538","type":"journal-article","created":{"date-parts":[[2022,4,23]],"date-time":"2022-04-23T07:55:10Z","timestamp":1650700510000},"page":"239-255","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":123,"title":["Intestinal peroxisome proliferator\u2010activated receptor \u03b1\u2010fatty acid\u2010binding protein 1 axis modulates nonalcoholic steatohepatitis"],"prefix":"10.1097","volume":"77","author":[{"given":"Tingting","family":"Yan","sequence":"first","affiliation":[{"name":"Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuhong","family":"Luo","sequence":"additional","affiliation":[{"name":"Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nana","family":"Yan","sequence":"additional","affiliation":[{"name":"Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA"},{"name":"State Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keisuke","family":"Hamada","sequence":"additional","affiliation":[{"name":"Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nan","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, P.R. China"},{"name":"Key Laboratory of Remodeling\u2010Related Cardiovascular Diseases, Ministry of Education, Beijing, P.R. 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