{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,20]],"date-time":"2025-09-20T19:45:20Z","timestamp":1758397520398},"reference-count":35,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"published-print":{"date-parts":[[2002,10,1]]},"abstract":"<jats:p>Essential fatty acid (EFA) deficiency induces fat malabsorption, but the pathophysiological mechanism is unknown. Bile salts (BS) and EFA-rich biliary phospholipids affect dietary fat solubilization and chylomicron formation, respectively. We investigated whether altered biliary BS and\/or phospholipid secretion mediate EFA deficiency-induced fat malabsorption in mice. Free virus breed (FVB) mice received EFA-containing (EFA<jats:sup>+<\/jats:sup>) or EFA-deficient (EFA<jats:sup>\u2212<\/jats:sup>) chow for 8 wk. Subsequently, fat absorption, bile flow, and bile composition were determined. Identical dietary experiments were performed in multidrug resistance gene-2-deficient [ Mdr2<jats:sup>(\u2212\/\u2212)<\/jats:sup>] mice, secreting phospholipid-free bile. After 8 wk, EFA<jats:sup>\u2212<\/jats:sup>-fed wild-type [ Mdr2<jats:sup>(+\/+)<\/jats:sup>] and Mdr2<jats:sup>(\u2212\/\u2212)<\/jats:sup>mice were markedly EFA deficient [plasma triene (20:3n-9)-to-tetraene (20:4n-6) ratio &gt;0.2]. Fat absorption decreased (70.1 \u00b1 4.2 vs. 99.1 \u00b1 0.3%, P &lt; 0.001), but bile flow and biliary BS secretion increased in EFA<jats:sup>\u2212<\/jats:sup>mice compared with EFA<jats:sup>+<\/jats:sup>controls (4.87 \u00b1 0.36 vs. 2.87 \u00b1 0.29 \u03bcl \u00b7 min<jats:sup>\u22121<\/jats:sup>\u00b7 100 g body wt<jats:sup>\u22121<\/jats:sup>, P &lt; 0.001, and 252 \u00b1 30 vs. 145 \u00b1 20 nmol \u00b7 min<jats:sup>\u22121<\/jats:sup>\u00b7 100 g body wt<jats:sup>\u22121<\/jats:sup>, P &lt; 0.001, respectively). BS composition was similar in EFA<jats:sup>+<\/jats:sup>- and EFA<jats:sup>\u2212<\/jats:sup>-fed mice. Similar to EFA<jats:sup>\u2212<\/jats:sup>Mdr2<jats:sup>(+\/+)<\/jats:sup>mice, EFA<jats:sup>\u2212<\/jats:sup>Mdr2<jats:sup>(\u2212\/\u2212)<\/jats:sup>mice developed fat malabsorption associated with twofold increase in bile flow and BS secretion. Fat malabsorption in EFA<jats:sup>\u2212<\/jats:sup>mice is not due to impaired biliary BS or phospholipid secretion. We hypothesize that EFA deficiency affects intracellular processing of dietary fat by enterocytes.<\/jats:p>","DOI":"10.1152\/ajpgi.00094.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T19:56:26Z","timestamp":1425412586000},"page":"G900-G908","source":"Crossref","is-referenced-by-count":25,"title":["Fat malabsorption in essential fatty acid-deficient mice is not due to impaired bile formation"],"prefix":"10.1152","volume":"283","author":[{"given":"Anniek","family":"Werner","sequence":"first","affiliation":[{"name":"Center for Liver, Digestive, and Metabolic Diseases, Pediatric Gastroenterology, Department of Pediatrics, University Hospital, 9700 RB Groningen, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Deanna M.","family":"Minich","sequence":"additional","affiliation":[{"name":"Center for Liver, Digestive, and Metabolic Diseases, Pediatric Gastroenterology, Department of Pediatrics, University Hospital, 9700 RB Groningen, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rick","family":"Havinga","sequence":"additional","affiliation":[{"name":"Center for Liver, Digestive, and Metabolic Diseases, Pediatric Gastroenterology, Department of Pediatrics, University Hospital, 9700 RB Groningen, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vincent","family":"Bloks","sequence":"additional","affiliation":[{"name":"Center for Liver, Digestive, and Metabolic Diseases, Pediatric Gastroenterology, Department of Pediatrics, University Hospital, 9700 RB Groningen, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Harry","family":"Van Goor","sequence":"additional","affiliation":[{"name":"Center for Liver, Digestive, and Metabolic Diseases, Pediatric Gastroenterology, Department of Pediatrics, University Hospital, 9700 RB Groningen, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Folkert","family":"Kuipers","sequence":"additional","affiliation":[{"name":"Center for Liver, Digestive, and Metabolic Diseases, Pediatric Gastroenterology, Department of Pediatrics, University Hospital, 9700 RB Groningen, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Henkjan J.","family":"Verkade","sequence":"additional","affiliation":[{"name":"Center for Liver, Digestive, and Metabolic Diseases, Pediatric Gastroenterology, Department of Pediatrics, University Hospital, 9700 RB Groningen, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"773","DOI":"10.1016\/S0021-9258(18)72862-7","volume":"140","author":"Barnes RH","year":"1941","journal-title":"J Biol 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