Wahlberg G, Walldius G, Efendic S
King Gustaf V Research Institute, Karolinska Hospital, Stockholm, Sweden.
Scand J Clin Lab Invest. 1992 Oct;52(6):537-45. doi: 10.3109/00365519209090131.
Nicotinic acid 4 g daily was given to 28 weight-stable hypertriglyceridaemic patients. The aim was to study its effects on serum lipoprotein lipid levels, intravenous glucose tolerance (k-values) and glucose incorporation into subcutaneous adipose tissue (GLIAT) in vitro. The investigations were performed prior to the nicotinic acid therapy, after 6 weeks, and 6 months of drug treatment. Fasting blood glucose levels increased by 13%, whereas k-values fell by 26% after the nicotinic acid treatment. Decrease in k-values was predicted from the initial k-values (R2-value = 0.76). GLIAT increased by 76%, while in the subgroup of eight patients, treated for 6 months with nicotinic acid, GLIAT increased by 331%. The changes in k-values and GLIAT were not significantly interrelated. Serum triglyceride levels were strongly decreased. The most likely explanation for the decrease in intravenous glucose tolerance is that nicotinic acid stimulates glucose output from the liver and that this effect outweighs the stimulating effects of the drug on glucose utilization in extrahepatic tissues. The latter is reflected by the increased uptake of glucose in adipose tissue. A stimulated GLIAT, reflecting formation of alpha-glycerophosphate in adipose tissue, might contribute to the reduction of serum triglyceride levels induced by nicotinic acid, since alpha-glycerophosphate is the acceptor of fatty acids assumed to be liberated from circulating triglycerides by lipoprotein lipase.
对28名体重稳定的高甘油三酯血症患者每日给予4克烟酸。目的是研究其对血清脂蛋白脂质水平、静脉葡萄糖耐量（k值）以及体外葡萄糖掺入皮下脂肪组织（GLIAT）的影响。在烟酸治疗前、治疗6周后以及6个月后进行了相关研究。烟酸治疗后，空腹血糖水平升高了13%，而k值下降了26%。k值的下降可根据初始k值预测（R²值 = 0.76）。GLIAT升高了76%，而在接受烟酸治疗6个月的8名患者亚组中，GLIAT升高了331%。k值和GLIAT的变化没有显著的相关性。血清甘油三酯水平大幅下降。静脉葡萄糖耐量降低最可能的解释是烟酸刺激肝脏葡萄糖输出，且这种作用超过了药物对肝外组织葡萄糖利用的刺激作用。后者通过脂肪组织中葡萄糖摄取增加得以体现。受刺激的GLIAT反映了脂肪组织中α - 甘油磷酸的形成，这可能有助于烟酸诱导的血清甘油三酯水平降低，因为α - 甘油磷酸是假定由脂蛋白脂肪酶从循环甘油三酯中释放出的脂肪酸的受体。
