Department of Nutritional Science, National Institute of Health and Nutrition, Tokyo, Japan.
Department of Nutritional Science, National Institute of Health and Nutrition, Tokyo, Japan.
J Lipid Res. 2012 Oct;53(10):2024-2037. doi: 10.1194/jlr.M023713. Epub 2012 Jun 26.
Postprandial hyperlipidemia (lipemia) is a risk factor for atherosclerosis. However, mouse models of postprandial hyperlipidemia have not been reported. Here, we report that ddY mice display marked postprandial hypertriglyceridemia in response to dietary fat. In ddY mice, the fasting serum total triacylglyceride (TG) concentration was 134 mg/dl, which increased to 571 mg/dl after an intragastric safflower oil load (0.4 ml/mouse). In C57BL/6J mice, these concentrations were 57 and 106 mg/dl, respectively. By lipoprotein analysis, ddY mice showed increases in chylomicron- and VLDL-sized TG fractions (remnants and VLDL) after fat load. In C57BL/6J mice, post-heparin plasma LPL activity after fat load was increased 4.8-fold relative to fasting. However, in ddY mice, the increase of LPL activity after fat load was very small (1.2-fold) and not significant. High fat feeding for 10 weeks led to obesity in ddY mice. A difference in LPL amino acid composition between C57BL/6J and ddY mice was detected but was deemed unlikely to cause hypertriglyceridemia because hypertriglyceridemia was not evident in other strains harboring the ddY-type LPL sequence. These findings indicate that postprandial hypertriglyceridemia in ddY mice is induced by decreased LPL activity after fat load and is associated with obesity induced by a high-fat diet.
餐后高脂血症(脂血)是动脉粥样硬化的一个危险因素。然而,尚未有报道过餐后高脂血症的小鼠模型。在这里,我们报道 ddY 小鼠对膳食脂肪表现出明显的餐后高甘油三酯血症。在 ddY 小鼠中,空腹血清总三酰甘油(TG)浓度为 134mg/dl,经胃内红花油负荷(0.4ml/只)后增加至 571mg/dl。在 C57BL/6J 小鼠中,这些浓度分别为 57 和 106mg/dl。通过脂蛋白分析,ddY 小鼠在脂肪负荷后显示出乳糜微粒和 VLDL 大小的 TG 分数(残粒和 VLDL)增加。在 C57BL/6J 小鼠中,脂肪负荷后肝素后血浆脂蛋白脂肪酶(LPL)活性比空腹时增加了 4.8 倍。然而,在 ddY 小鼠中,脂肪负荷后 LPL 活性的增加非常小(1.2 倍)且不显著。高脂喂养 10 周导致 ddY 小鼠肥胖。在 C57BL/6J 和 ddY 小鼠之间检测到 LPL 氨基酸组成的差异,但由于在携带 ddY 型 LPL 序列的其他品系中没有明显的高甘油三酯血症,因此不太可能导致高甘油三酯血症。这些发现表明,ddY 小鼠的餐后高甘油三酯血症是由脂肪负荷后 LPL 活性降低引起的,与高脂肪饮食引起的肥胖有关。