Agbedana E O, Johnson A O, Taylor G O
Am J Clin Nutr. 1979 Feb;32(2):292-8. doi: 10.1093/ajcn/32.2.292.
Postheparin serum lipolytic activities (hepatic and extrahepatic), serum free fatty acid, and triglyceride levels were measured in 16 kwashiorkor, 14 marasmic, and 14 control children. The results showed that the reduction in total postheparin lipolytic activity in kwashiorkor was in the activity of hepatic origin. In marasmus, the total postheparin lipolytic activity, hepatic and extrahepatic activities, were within normal range. The was no evidence for the presence of inhibitors of postheparin lipolytic activity in the serum of kwashiorkor or marasmic children. Fasting serum-free fatty acid level was significantly elevated in kwashiorkor, while the level in marasmus was not significantly different from control value. The serum triglyceride levels in both conditions showed no significant differences from the control value. These findings suggest that the defective production of hepatic lipoprotein lipase, as well as increased influx of free fatty acid into the liver, could account for the accumulation of fat in the liver of kwashiorkor and not in that of marasmic children.
对16名夸休可尔症患儿、14名消瘦症患儿和14名对照儿童测定了肝素化后血清脂解活性（肝源性和肝外性）、血清游离脂肪酸和甘油三酯水平。结果显示，夸休可尔症患儿肝素化后总脂解活性的降低在于肝源性活性。在消瘦症中，肝素化后总脂解活性、肝源性和肝外性活性均在正常范围内。没有证据表明夸休可尔症或消瘦症患儿血清中存在肝素化后脂解活性抑制剂。夸休可尔症患儿空腹血清游离脂肪酸水平显著升高，而消瘦症患儿的该水平与对照值无显著差异。两种情况下的血清甘油三酯水平与对照值均无显著差异。这些发现表明，肝脂蛋白脂肪酶产生缺陷以及游离脂肪酸流入肝脏增加，可能是夸休可尔症患儿肝脏脂肪蓄积的原因，而消瘦症患儿肝脏则不然。
