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Hepatic lipogenesis and a marker of hepatic lipid oxidation, predict postprandial responses of triglyceride‐rich lipoproteins
Author(s) -
Matikainen Niina,
Adiels Martin,
Söderlund Sanni,
Stennabb Sanna,
Ahola Tytti,
Hakkarainen Antti,
Borén Jan,
Taskinen MarjaRiitta
Publication year - 2014
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.20781
Subject(s) - postprandial , lipogenesis , triglyceride , medicine , triglycerides blood , endocrinology , chemistry , lipid metabolism , cholesterol , insulin
Objective 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. Methods 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. Results 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. Conclusions 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.