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[奶牛肝脏脂质osis:第1部分 - 胰岛素和生长激素 - IGF-1轴的作用]

[The lipidosis of the liver of dairy cows: Part 1 - Role of insulin and the Growth Hormone-IGF-1 axis].

作者信息

Martens Holger

机构信息

Institut für Veterinär-Physiologie, Freie Universität Berlin.

出版信息

Tierarztl Prax Ausg G Grosstiere Nutztiere. 2023 Apr;51(2):97-108. doi: 10.1055/a-2066-2596. Epub 2023 May 25.

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).

摘要

奶牛肝脏脂肪变性是一种多年来为人所知的代谢性疾病,其病因是肝细胞摄取非酯化脂肪酸(NEFA)、NEFA代谢受限(氧化及β-羟基丁酸生成)以及相对于作为甘油三酯(TG)的低流出量的再合成。脂肪变性的发病机制包括:a)通过脂肪组织动员增加NEFA释放;b)NEFA进入肝细胞;c)NEFA代谢;d)甘油三酯再合成;e)TG以极低密度脂蛋白(VLDL)形式流出。产后,步骤a至e会受到激素影响而改变,如生长激素增加、明显的胰岛素抵抗以及胰岛素和IGF-1浓度降低。这些激素变化与生长激素-IGF-1轴解偶联有关,伴有脂解增强及上述后果。这些改变与炎症、氧化应激和内质网应激相关。代谢和激素改变是主要为产奶而选择奶牛但食物摄入不足的结果,会导致脂肪变性、酮病及其他健康风险(生产性疾病)。

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