Fasting hypertriglyceridemia in noninsulin-dependent diabetes mellitus is an important predictor of postprandial lipid and lipoprotein abnormalities.
Fasting hypertriglyceridemia in noninsulin-dependent diabetes mellitus is an important predictor of postprandial lipid and lipoprotein abnormalities.
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DOI：
10.1210/jcem-72-4-934
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发表时间：
1991-04
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影响因子：
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通讯作者：
G. Lewis;N. O'Meara;P. Soltys;J. Blackman;P. Iverius;W. Pugh;G. Getz;K. Polonsky
中科院分区：
文献类型：
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作者：
G. Lewis;N. O'Meara;P. Soltys;J. Blackman;P. Iverius;W. Pugh;G. Getz;K. Polonsky
餐后脂蛋白代谢可能在动脉粥样硬化形成中起重要作用，但在非胰岛素依赖型糖尿病（NIDDM）中尚未进行详细研究。我们使用维生素A脂肪负荷试验来标记12名未经治疗的NIDDM患者在摄入含有60 g脂肪/m2和60，000 U维生素A/m2的高脂肪混合餐后肠源性的富含维生素A的脂蛋白颗粒（NTG;甘油三酯，低于1.7 mmol/L），7例未接受治疗的NIDDM受试者伴中度高甘油三酯血症（HTG;甘油三酯，1.7-4.7 mmol/L），和8个年龄和体重匹配的血糖正常的非糖尿病对照组。餐后甘油三酯增量在NIDDM伴HTG组更大（P = 0.0001），并且在所有组中与空腹甘油三酯浓度密切相关（r = 0.83; P = 0.0001）。在全血浆中测得的棕榈酸视黄酯、大于1000乳糜微粒分数的Sf和小于1000非乳糜微粒分数的Sf在NIDDM合并HTG中也显著更高，但在NIDDM合并NTG和对照组之间没有显著差异。在伴有HTG的NIDDM患者中，乳糜微粒的清除速度较慢，这一点可通过乳糜微粒和非乳糜微粒棕榈酸视黄酯反应曲线的交叉时间明显较晚得到证明（HTG NIDDM患者为13.7 h，NTG NIDDM患者为8.5 h，对照组为7.3 h; P <0.01）。尽管三组受试者的空腹FFA水平相似，但HTG糖尿病受试者的FFA在餐后出现晚期高峰，持续时间长达14小时。各组餐后FFA升高与空腹甘油三酯浓度（r = 0.57; P <0.002）和餐后甘油三酯升高（r = 0.80; P = 0.0001）相关。NIDDM伴HTG组HDL颗粒的空腹核心甘油三酯含量显著高于NIDDM伴NTG组和对照组（分别为21.0%和14.0%和14.1%; P <0.05），并且这在所有组中在餐后以胆固醇酯为代价增加了比例，增加与餐后总血浆甘油三酯增加相关（r = 0.51; P <0.01）。我们的结论是，中度空腹高脂血症的NIDDM是一个星座的预测餐后血脂和脂蛋白的变化，可能会加强已经不利的动脉粥样硬化空腹血脂谱在这些科目。
Postprandial lipoprotein metabolism may be important in atherogenesis and has not been studied in detail in noninsulin-dependent diabetes mellitus (NIDDM). We used the vitamin A fat-loading test to label triglyceride-rich lipoprotein particles of intestinal origin after ingestion of a high fat mixed meal containing 60 g fat/m2 and 60,000 U vitamin A/m2 in 12 untreated NIDDM subjects with normotriglyceridemia (NTG; triglycerides, less than 1.7 mmol/L), 7 untreated NIDDM subjects with moderate hypertriglyceridemia (HTG; triglycerides, 1.7-4.7 mmol/L), and 8 age- and weight-matched normotriglyceridemic nondiabetic controls. The postprandial triglyceride increment was greater in NIDDM with HTG (P = 0.0001) and correlated strongly in all groups with the fasting triglyceride concentration (r = 0.83; P = 0.0001). Retinyl palmitate measured in whole plasma, an Sf greater than 1000 chylomicron fraction, and an Sf less than 1000 nonchylomicron fraction was also significantly greater in NIDDM with HTG, but did not differ significantly between NIDDM with NTG and controls. In NIDDM with HTG, chylomicrons appeared to be cleared at a slower rate, as evidenced by the significantly later intersection of the chylomicron and nonchylomicron retinyl palmitate response curves (13.7 h in HTG NIDDM vs. 8.5 h in NTG NIDDM vs. 7.3 h in controls; P less than 0.01). Although fasting FFA levels were similar in all three groups, the HTG diabetic subjects had a late postprandial surge in FFAs that lasted for up to 14 h. The postprandial FFA elevation in all groups correlated with the fasting triglyceride concentration (r = 0.57; P less than 0.002) and postprandial triglyceride increment (r = 0.80; P = 0.0001). The fasting core triglyceride content of the HDL particles in NIDDM with HTG was significantly elevated compared to those in NIDDM with NTG and controls (21.0% vs. 14.0% vs. 14.1% respectively; P less than 0.05), and this increased proportionately in all groups after the meal at the expense of cholesteryl ester, the increase correlating with total plasma postprandial triglyceride increment (r = 0.51; P less than 0.01). We conclude that moderate fasting hypertriglyceridemia in NIDDM is predictive of a constellation of postprandial changes in lipids and lipoproteins that may potentiate the already unfavorable atherogenic fasting lipid profile in these subjects.