Curtin A, Deegan P, Owens D, Collins P, Johnson A, Tomkin G H
Department of Clinical Medicine, Trinity College, Dublin, Ireland.
Acta Diabetol. 1995 Dec;32(4):244-50. doi: 10.1007/BF00576257.
We have previously demonstrated alterations in apolipoprotein B-48 metabolism in the post-prandial state in patients with non-insulin-dependent diabetes mellitus. This study investigates the relationship between hypertriglyceridaemia and post-prandial lipoprotein metabolism. Four groups of patients were examined: non-insulin-dependent diabetic patients, with normal serum triglyceride levels (serum triglyceride < 2.1 mmol l-1; haemoglobin HbA1c 5.5% +/- 0.4%); poorly controlled, non-insulin-dependent diabetic patients with hypertriglyceridaemia (serum triglyceride > 2.1 mmol l-1; HbA1c 8.8% +/- 0.9%); non-diabetic subjects with serum triglycerides < 2.1 mmol l-1; and non-diabetic subjects with hypertriglyceridaemia (serum triglyceride > 2.1 mmol l-1). Subjects were studied fasting and following a high-fat meal (1300 kcal). The triglyceride-rich lipoprotein fraction was isolated by ultracentrifugation (d < 1.006 g ml-1). Apoprotein B-48, apoprotein B-100 and apoprotein E were separated on 4%-15% gradient gels and quantified as a percentage of the fasting concentration by densitometric scanning. Triglyceride-rich lipoprotein apolipoprotein B-48 and apolipoprotein B-100 post-prandial profiles demonstrated a maximum increase either at 2 h or rising still further to a peak at 6 h before falling in the diabetic groups and hypertriglyceridaemic non-diabetic subjects when compared with the normotriglyceridaemic control subjects whose levels decreased after 2 h (P < 0.05). A significantly different triglyceride-rich lipoprotein apolipoprotein E profile was also exhibited by the diabetic patients (P < 0.05). Levels of triglyceride-rich lipoprotein, cholesterol, triglyceride, total protein and apoprotein B were elevated in the hypertriglyceridaemic subjects, both diabetic and non-diabetic. These results indicate that hypertriglyceridaemia is associated with altered metabolism and composition of post-prandial triglyceride-rich lipoprotein particles in both poorly controlled diabetic and non-diabetic subjects.
我们之前已证明非胰岛素依赖型糖尿病患者餐后载脂蛋白B-48代谢存在改变。本研究调查高甘油三酯血症与餐后脂蛋白代谢之间的关系。研究了四组患者:血清甘油三酯水平正常(血清甘油三酯<2.1 mmol/L;血红蛋白HbA1c 5.5%±0.4%)的非胰岛素依赖型糖尿病患者;控制不佳、伴有高甘油三酯血症(血清甘油三酯>2.1 mmol/L;HbA1c 8.8%±0.9%)的非胰岛素依赖型糖尿病患者;血清甘油三酯<2.1 mmol/L的非糖尿病受试者;以及伴有高甘油三酯血症(血清甘油三酯>2.1 mmol/L)的非糖尿病受试者。对受试者进行空腹研究,并在进食高脂餐(1300千卡)后进行研究。通过超速离心分离富含甘油三酯的脂蛋白部分(d<1.006 g/ml)。载脂蛋白B-48、载脂蛋白B-100和载脂蛋白E在4%-15%梯度凝胶上分离,并通过密度扫描定量为空腹浓度的百分比。与甘油三酯正常的对照组相比,糖尿病组和高甘油三酯血症非糖尿病受试者中,富含甘油三酯的脂蛋白载脂蛋白B-48和载脂蛋白B-100餐后曲线在2小时时出现最大增加,或在6小时时仍进一步上升至峰值,然后下降,而对照组在2小时后水平下降(P<0.05)。糖尿病患者的富含甘油三酯的脂蛋白载脂蛋白E曲线也有显著差异(P<0.05)。糖尿病和非糖尿病的高甘油三酯血症受试者中,富含甘油三酯的脂蛋白、胆固醇、甘油三酯、总蛋白和载脂蛋白B水平均升高。这些结果表明,高甘油三酯血症与控制不佳的糖尿病和非糖尿病受试者餐后富含甘油三酯的脂蛋白颗粒代谢和组成改变有关。