{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T22:06:15Z","timestamp":1764194775902,"version":"3.30.2"},"reference-count":128,"publisher":"Georg Thieme Verlag KG","issue":"02","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Tierarztl Prax Ausg G Grosstiere Nutztiere"],"published-print":{"date-parts":[[2023,4]]},"abstract":"<jats:title>Zusammenfassung<\/jats:title><jats:p>Die Fettleber von Milchk\u00fchen ist seit vielen Jahren bekannt und bedingt\n                    durch eine vermehrte Aufnahme von freien Fetts\u00e4uren (NEFA) in die\n                    Leberzellen und unzureichender Metabolisierung in Relation zur Abgabe der NEFA\n                    als resynthetisierte Triglyzeride (TG). Die Pathogenese der Fettleber umfasst a)\n                    eine erh\u00f6hte Lipolyse im Fettgewebe mit einem Anstieg der freien\n                    Fetts\u00e4uren (NEFA) Konzentration im Blut, b) die Aufnahme von NEFA in die\n                    Leberzellen proportional der Konzentration, c) die Metabolisierung der NEFA\n                    (Oxidation, Bildung von Ketonk\u00f6rpern), d) die erneute Synthese von TG\n                    bzw. von very low density lipoprotein (VLDL) und e) deren Abgabe. An diesen\n                    Schritten (a\u2013e) sind hormonelle Ver\u00e4nderungen ma\u00dfgeblich\n                    beteiligt. Es handelt sich um den Anstieg des Wachstumshormons (GH), eine\n                    ausgepr\u00e4gte Insulinresistenz in Verbindung mit einem Abfall der Insulin-\n                    und IGF-1-Konzentration im Blut. Als Folge dieser hormonellen\n                    Ver\u00e4nderungen ergibt sich mit steigender Milchleistung eine Entkoppelung\n                    der GH-IGF-1-Achse in der Leber mit einer vermehrten Lipolyse im Fettgewebe,\n                    Freisetzung von NEFA und den o.a. Konsequenzen. Diese Ver\u00e4nderungen sind\n                    assoziiert mit Entz\u00fcndungserscheinungen, oxidativen und\n                    endoplasmatischen Stress. Die hormonellen Ver\u00e4nderungen mit den\n                    metabolischen Konsequenzen sind das Ergebnis der prim\u00e4ren Selektion auf\n                    hohe Milchleistung ohne bedarfsgerechte Futteraufnahme und als Ursache der\n                    Pathogenese der Leberverfettung und Ketose und deren Folgeerkrankungen\n                    (\u201eProduktionskrankheiten\u201c) anzusehen.<\/jats:p>","DOI":"10.1055\/a-2066-2596","type":"journal-article","created":{"date-parts":[[2023,5,25]],"date-time":"2023-05-25T22:53:53Z","timestamp":1685055233000},"page":"97-108","source":"Crossref","is-referenced-by-count":3,"title":["Die Leberverfettung der Milchkuh: Teil 1"],"prefix":"10.1055","volume":"51","author":[{"given":"Holger","family":"Martens","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Veterin\u00e4r-Physiologie, Freie\n                    Universit\u00e4t Berlin"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"194","published-online":{"date-parts":[[2023,5,25]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"281","DOI":"10.1136\/yr107.12.281","article-title":"Incidence and severity of fatty liver in dairy cows","volume":"197","author":"I. 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