Matikainen Niina, Adiels Martin, Söderlund Sanni, Stennabb Sanna, Ahola Tytti, Hakkarainen Antti, Borén Jan, Taskinen Marja-Riitta
Department of Medicine, Cardiovascular Research Unit, Diabetes and Obesity Research Program, Heart and Lung Center, University of Helsinki, Finland; Division of Endocrinology, Helsinki University Central Hospital, University of Helsinki, Finland.
Obesity (Silver Spring). 2014 Aug;22(8):1854-9. doi: 10.1002/oby.20781. Epub 2014 May 28.
Postprandial hypertriglyceridemia is an important risk factor for cardiovascular disease. The mechanisms are still unclear. Here it was tested if hepatic de novo lipogenesis (DNL) and lipid oxidation influence the postprandial responses of triglyceride-rich lipoproteins (TRL) in humans.
The contribution of hepatic DNL to hepatic TRL production was analyzed in 67 men and women with a moderate range of BMI after a fat-rich meal. Also, lipase activities, liver fat, and 3-OH-butyrate were quantitated as an indicator of β-oxidation. Lipoproteins and metabolic markers were measured in fasting and postprandial blood samples.
Postprandial DNL correlates with postprandial TG and apolipoprotein (apo) C-III responses in plasma and with TG, apoB48 and apoB100 responses in TRLs and their larger remnant particles. Fasting and 8-h postprandial DNL was inversely related to 3-OH-butyrate but not to liver fat content. Fasting apoC-III and 3-OH-butyrate, but not liver fat, independently predicted fasting DNL.
The fasting and 8-h postprandial rate of DNL was inversely associated with the hepatic lipid oxidation in humans. DNL contributes significantly to the TG content in TRLs but not to the amount of liver fat, suggesting that an imbalance between DNL and fat oxidation contributes to postprandial atherogenic dyslipidemia.
餐后高甘油三酯血症是心血管疾病的一个重要危险因素。其机制仍不清楚。本研究旨在检测肝脏从头脂肪生成（DNL）和脂质氧化是否影响人类富含甘油三酯脂蛋白（TRL）的餐后反应。
对67名BMI处于中等范围的男性和女性在进食富含脂肪的餐后，分析肝脏DNL对肝脏TRL产生的贡献。此外，定量测定脂肪酶活性、肝脏脂肪和3-羟基丁酸作为β氧化的指标。在空腹和餐后血样中测量脂蛋白和代谢标志物。
餐后DNL与血浆中餐后甘油三酯（TG）和载脂蛋白（apo）C-III反应以及TRL及其较大残粒颗粒中的TG、apoB48和apoB100反应相关。空腹和餐后8小时的DNL与3-羟基丁酸呈负相关，但与肝脏脂肪含量无关。空腹apoC-III和3-羟基丁酸，而非肝脏脂肪，独立预测空腹DNL。
人类空腹和餐后8小时的DNL速率与肝脏脂质氧化呈负相关。DNL对TRL中的TG含量有显著贡献，但对肝脏脂肪量无贡献，这表明DNL与脂肪氧化之间的失衡导致餐后致动脉粥样硬化性血脂异常。
