Childs M T, Tollefson J, Knopp R H, Bowden D A
Metabolism. 1981 Jan;30(1):27-35. doi: 10.1016/0026-0495(81)90214-6.
We have asked, is hypertriglyceridemia in the fed state in pregnancy due to intolerance to exogenous fat, accumulation of endogenous triglycerides, or accumulation of remnants of d < 1.006 lipoprotein metabolism? To answer these questions, we fed fat-free diets high in starch or sucrose, or diets containing fat or fat plus cholesterol to pregnant and nonpregnant rats for 12 days until gestational day 21 (term = 22 days). Blood was obtained 0, 4, or 8 hr after removal of food from the cages. Lipid concentrations were determined in chylomicrons and very low, low, and high density lipoproteins. Hypertriglyceridemia in pregnancy exists on both starch and sucrose containing fat-free diets and is exaggerated 4 and 8 hr after food is removed from the cage. The triglyceride rise occurs in d < 1.006 lipoproteins. With fat feeding, chylomicron triglyceride concentrations are not significantly elevated in pregnant rats, 0 or 8 hr postabsorptively despite greater food intake in pregnancy. In contrast, very low density lipoprotein (VLDL) triglyceride concentrations are elevated at all times following fat feeding in pregnant compared to nonpregnant animals. A significant contribution of lipoprotein remnants to the triglyceride rise in d < 1.006 lipoproteins seems unlikely since an isolated increase in VLDL cholesterol is not observed. No statistically significant accumulation of hepatic triglycerides occurs on any diet in pregnancy. Diet induced shifts in adipose tissue and muscle lipoprotein lipase activity are exaggerated in pregnancy while hepatic lipase is unaffected. Fetal weight is similar on all diets except sucrose where weight is reduced.
Hypertriglyceridemia in fed pregnant rats is due to an increase in endogenous triglycerides. Remnant lipid accumulation does not appear to contribute to the endogenous hypertriglyceridemia. There is no intolerance to exogenous (dietary) fat. The results are compatible with an unimpaired delivery of exogenous fat to fat oxidizing tissues thereby maximizing glucose availability for fetal growth.
我们提出了这样的问题，孕期进食状态下的高甘油三酯血症是由于对外源性脂肪不耐受、内源性甘油三酯蓄积，还是由于密度小于1.006的脂蛋白代谢残余物蓄积所致？为回答这些问题，我们给怀孕和未怀孕的大鼠喂食高淀粉或高蔗糖的无脂饮食，或含脂肪或脂肪加胆固醇的饮食，持续12天直至妊娠第21天（足月为22天）。从笼中取出食物后0、4或8小时采集血液。测定乳糜微粒以及极低密度、低密度和高密度脂蛋白中的脂质浓度。孕期在含淀粉和蔗糖的无脂饮食中均存在高甘油三酯血症，且在从笼中取出食物后4小时和8小时更为明显。甘油三酯升高发生在密度小于1.006的脂蛋白中。喂食脂肪后，尽管孕期食物摄入量增加，但吸收后0小时或8小时怀孕大鼠的乳糜微粒甘油三酯浓度并未显著升高。相比之下，与未怀孕动物相比，怀孕动物喂食脂肪后，极低密度脂蛋白（VLDL）甘油三酯浓度在所有时间均升高。由于未观察到VLDL胆固醇单独升高，脂蛋白残余物对密度小于1.006的脂蛋白中甘油三酯升高的显著贡献似乎不太可能。孕期任何饮食均未出现肝脏甘油三酯的统计学显著蓄积。饮食诱导的脂肪组织和肌肉脂蛋白脂肪酶活性变化在孕期更为明显，而肝脏脂肪酶未受影响。除蔗糖饮食导致体重减轻外，所有饮食组的胎儿体重相似。
喂食状态下怀孕大鼠的高甘油三酯血症是由于内源性甘油三酯增加所致。残余脂质蓄积似乎并未导致内源性高甘油三酯血症。对外源性（饮食）脂肪不存在不耐受。这些结果与外源性脂肪向脂肪氧化组织的正常输送相符，从而使胎儿生长的葡萄糖可利用性最大化。
