Walzem R L, Davis P A, Hansen R J
Department of Molecular Biosciences, School of Veterinary Medicine, University of California-Davis 95616.
J Lipid Res. 1994 Aug;35(8):1354-66.
Structurally specific very low density lipoprotein (VLDL) particles are presumed to redirect VLDL uptake during yolk deposition. Egg production is an energy intensive process, but energy excess negatively affects egg production. This study sought to determine whether overfeeding changed hen lipoprotein profiles, and if so, whether changes were related to egg production. Overfeeding caused 33% of hens to stop yolk deposition and reabsorb unovulated follicles (involute). VLDL of control hens possessed characteristic small particle size (30 nm) and composition indicative of limited intravascular metabolism. Overfeeding generally increased VLDL diameter, the effect being slight (+6.6 nm) in overfed laying hens when compared to overfed-involuted hens (+51.2 nm). Changes in composition indicated that increased intravascular metabolism of VLDL parallelled increases in particle diameter. Overfed-involuted hens showed significant elevations of plasma low density lipoprotein, VLDL cholesteryl ester, and high density lipoprotein (HDL) triacylglycerol content. Overfeeding increased plasma HDL, and in association with involution, caused redistribution of HDL particle sizes, including the appearance of novel HDL approximately 20 nm in diameter, termed HDLR, and a 97 kDa protein within the HDL fraction. The overfed hen model may provide new insight into the role of lipoprotein physical properties in determining the metabolism of triacylglycerol-rich lipoprotein, and the process of reverse lipid transport. Overfeeding generally increases VLDL size and plasma HDL levels suggesting that increased peripheral metabolism, and perhaps mechanical exclusion of enlarged VLDL by the granulosa basal lamina, contribute to the obesity and impaired yolk deposition observed in hens with excessive energy intakes. Temporal definition of massive VLDL enlargement relative to follicular collapse remains to be established.(ABSTRACT TRUNCATED AT 250 WORDS)
结构特异性极低密度脂蛋白(VLDL)颗粒被认为在卵黄沉积过程中重新引导VLDL的摄取。产蛋是一个能量密集型过程,但能量过剩会对产蛋产生负面影响。本研究旨在确定过度喂养是否会改变母鸡的脂蛋白谱,如果是,这些变化是否与产蛋有关。过度喂养导致33%的母鸡停止卵黄沉积并重新吸收未排卵的卵泡(退化)。对照母鸡的VLDL具有特征性的小粒径(30纳米)和表明血管内代谢有限的组成。过度喂养通常会增加VLDL直径,与过度喂养后卵泡退化的母鸡(增加51.2纳米)相比,过度喂养的产蛋母鸡的这种影响较小(增加6.6纳米)。组成变化表明,VLDL血管内代谢的增加与粒径的增加平行。过度喂养后卵泡退化的母鸡血浆低密度脂蛋白、VLDL胆固醇酯和高密度脂蛋白(HDL)三酰甘油含量显著升高。过度喂养会增加血浆HDL,并与卵泡退化相关,导致HDL粒径重新分布,包括出现直径约20纳米的新型HDL,称为HDLR,以及HDL组分中的一种97千道尔顿蛋白。过度喂养的母鸡模型可能为脂蛋白物理性质在决定富含三酰甘油脂蛋白代谢和逆向脂质转运过程中的作用提供新的见解。过度喂养通常会增加VLDL大小和血浆HDL水平,这表明外周代谢增加,可能还有颗粒细胞基膜对增大的VLDL的机械排斥,导致能量摄入过多的母鸡出现肥胖和卵黄沉积受损。相对于卵泡塌陷的大量VLDL增大的时间定义仍有待确定。(摘要截短于250字)