Nikkilä E A, Huttunen J K, Ehnholm C
Diabetes. 1977 Jan;26(1):11-21. doi: 10.2337/diab.26.1.11.
The activity of two triglyceride lipases was determined by an immunochemical method in the postheparin plasma of 60 diabetic patients and of 47 age- and sex-matched nondiabetic control subjects. The results were related to the type of diabetes, to plasma triglyceride and insulin concentrations, to removal of exogenous fat from the blood, and to turnover of VLDL-triglycerides . The mean postheparin plasma lipoprotein lipase (LPL) activity was decreased by 44 per cent (p less than 0.001) in patients with untreated ketotic diabetes and by 20 per cent (p less than 0.01) in patients with untreated mild to moderate nonketotic early-onset diabetes. Insulin treatment of ketotic diabetes resulted in a rapid increase in the activity of LPL and decrease in serum triglycerdie level, whereas sulfonylurea treatment of non-insulin-requiring diabetics did not significantly influence the enzyme activity. In insulin-treated chronic diabetics the average postheparin plasma LPL activity was not different from that of nondiabetic controls, but some of these patients had high LPL values. In normolipidemic maturity-onset-type diabetics the LPL activity was within normal range, but in those having hypertriglyceridemia the average LPL value was decreased by an average of 26 per cent (p less than 0.01). The LPL activity showed a significant negative correlation with the logarithm of serum triglyceride concentration (r = -0.62) and a positive correlation with fractional removal of Intralipid (r = +0.64) and fractional turnover of V triglyceride (r = +0.40). The activity of LPL was correlated to basal plasma insulin concen tration in the insulin-deficient diabetes r = +0.34) but not in patients with maturity-onset-type diabetes. The hepatic lipase (HL) activity of postheparin plasma was similar in diabetes and controls, with the exception of hypertriglyceridemic maturity-onset diabetics, who had higher mean HL activity than the corresponding control group (p greater than 0.01). The activity of HL was not related to triglyceride removal but showed a significant correlation to VLDL-triglyceride production rate. On the basis of these results it seems that a deficiency of LPL accounts for a great deal of the elevation of serum triglyceride in insulin-deficient human diabetes but has a smaller role in the pathogenesis of the hypertriglyceridemia that is associated with maturity-onset diabetes. The latter abnormality is caused mainly by an increased secretion of triglycerides into the blood even though a decreased LPL may contribute to development of hyperlipemia in cases with gross elevation of serum triglycerides.
采用免疫化学方法测定了60例糖尿病患者及47例年龄和性别匹配的非糖尿病对照者肝素后血浆中两种甘油三酯脂肪酶的活性。结果与糖尿病类型、血浆甘油三酯和胰岛素浓度、血液中外源性脂肪的清除以及极低密度脂蛋白甘油三酯的周转率相关。未治疗的酮症糖尿病患者肝素后血浆脂蛋白脂肪酶（LPL）活性平均降低44%（p<0.001），未治疗的轻度至中度非酮症早发糖尿病患者降低20%（p<0.01）。酮症糖尿病患者接受胰岛素治疗后，LPL活性迅速升高，血清甘油三酯水平降低，而磺脲类药物治疗非胰岛素依赖型糖尿病患者对酶活性无显著影响。胰岛素治疗的慢性糖尿病患者肝素后血浆LPL活性平均与非糖尿病对照者无差异，但其中一些患者LPL值较高。血脂正常的成年发病型糖尿病患者LPL活性在正常范围内，但甘油三酯血症患者的平均LPL值平均降低26%（p<0.01）。LPL活性与血清甘油三酯浓度的对数呈显著负相关（r=-0.62），与脂肪乳剂的分数清除率呈正相关（r=+0.64），与极低密度脂蛋白甘油三酯的分数周转率呈正相关（r=+0.40）。LPL活性在胰岛素缺乏型糖尿病中与基础血浆胰岛素浓度相关（r=+0.34），但在成年发病型糖尿病患者中无相关性。肝素后血浆肝脂酶（HL）活性在糖尿病患者和对照者中相似，但甘油三酯血症成年发病型糖尿病患者除外，其平均HL活性高于相应对照组（p>0.01）。HL活性与甘油三酯清除无关，但与极低密度脂蛋白甘油三酯生成率呈显著相关。基于这些结果，似乎LPL缺乏在胰岛素缺乏型人类糖尿病患者血清甘油三酯升高中起很大作用，但在与成年发病型糖尿病相关的高甘油三酯血症发病机制中作用较小。后者的异常主要是由于甘油三酯分泌入血增加所致，尽管LPL降低可能在血清甘油三酯显著升高的情况下促进高脂血症的发展。
