Tierarztl Prax Ausg G Grosstiere Nutztiere 2023; 51(02): 97-108
DOI: 10.1055/a-2066-2596
Übersichtsartikel

Die Leberverfettung der Milchkuh: Teil 1

Bedeutung von Insulin und der Wachstumshormon-IGF-1-AchseThe lipidosis of the liver of dairy cows: Part 1Role of insulin and the Growth Hormone-IGF-1 axis
Holger Martens
1   Institut für Veterinär-Physiologie, Freie Universität Berlin
› Author Affiliations

Zusammenfassung

Die Fettleber von Milchkühen ist seit vielen Jahren bekannt und bedingt durch eine vermehrte Aufnahme von freien Fettsäuren (NEFA) in die Leberzellen und unzureichender Metabolisierung in Relation zur Abgabe der NEFA als resynthetisierte Triglyzeride (TG). Die Pathogenese der Fettleber umfasst a) eine erhöhte Lipolyse im Fettgewebe mit einem Anstieg der freien Fettsäuren (NEFA) Konzentration im Blut, b) die Aufnahme von NEFA in die Leberzellen proportional der Konzentration, c) die Metabolisierung der NEFA (Oxidation, Bildung von Ketonkörpern), d) die erneute Synthese von TG bzw. von very low density lipoprotein (VLDL) und e) deren Abgabe. An diesen Schritten (a–e) sind hormonelle Veränderungen maßgeblich beteiligt. Es handelt sich um den Anstieg des Wachstumshormons (GH), eine ausgeprägte Insulinresistenz in Verbindung mit einem Abfall der Insulin- und IGF-1-Konzentration im Blut. Als Folge dieser hormonellen Veränderungen ergibt sich mit steigender Milchleistung eine Entkoppelung der GH-IGF-1-Achse in der Leber mit einer vermehrten Lipolyse im Fettgewebe, Freisetzung von NEFA und den o.a. Konsequenzen. Diese Veränderungen sind assoziiert mit Entzündungserscheinungen, oxidativen und endoplasmatischen Stress. Die hormonellen Veränderungen mit den metabolischen Konsequenzen sind das Ergebnis der primären Selektion auf hohe Milchleistung ohne bedarfsgerechte Futteraufnahme und als Ursache der Pathogenese der Leberverfettung und Ketose und deren Folgeerkrankungen („Produktionskrankheiten“) anzusehen.

Abstract

Lipidosis of the liver of dairy cows is a metabolic disease known since many years and is caused by an uptake of nonesterified fatty acids (NEFA) into the liver cells, limited metabolism of NEFA (oxidation and production of β-hydroxybutyrate), and resynthesis in relation to a low efflux as triglyceride (TG). The pathogenesis of lipidosis includes a) an augmented release of NEFA by mobilisation of adipose tissue, b) uptake of NEFA into the liver cells, c) metabolism of NEFA and d) re-synthesis of triglyceride and e) an efflux of TG as very low density lipoprotein (VLDL). The steps a–e are postpartum modified by hormones as an increase of growth hormone, a pronounced insulin resistance in combination with a decreased insulin and of IGF-1 concentrations. These hormonal changes are related to an uncoupling of the growth hormone-IGF-1-axis with enhanced lipolysis and consequences mentioned above. These alterations are associated with inflammation, oxidative and endoplasmatic stress. The metabolic and hormonal alterations are the result of the selection of dairy cows primarily for milk production without adequate food intake with the consequence of lipidosis, ketosis and further health risks (production diseases).



Publication History

Received: 16 August 2022

Accepted: 27 March 2023

Article published online:
25 May 2023

© 2023. Thieme. All rights reserved.

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