Postprandial factor VII activation does not increase plasma concentrations of prothrombin fragment 1 + 2 in patients with morbid obesity

Line Espenhain Landgrebe*, Claus Bogh Juhl, Vibeke Andersen, Lucas Moitinho-Silva, Corinna Bang, Else Marie Bladbjerg

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review


Introduction: Increased postprandial factor VII activation is observed after high-fat meals, but is not accompanied by thrombin formation in normal weight individuals. Obesity is associated with a higher circulating concentration of tissue factor (TF) and postprandial uptake of lipopolysaccharide (LPS), and this may increase thrombin formation after high-fat meals. We therefore compared postprandial effects of high-fat meals and low-fat meals on biomarkers of coagulation activation in patients with morbid obesity and investigated whether the response was associated with the gut bacteria composition. Materials and methods: A controlled cross-over study was conducted in obese patients (15 women, 5 men, mean BMI = 44.1 kg/m2), where high-fat meals (67 E% fat) and low-fat meals (16 E% fat) were served at 8:15 and 10:00 in a random order on two study days within one week. Blood samples were collected at 08:00 (fasting), 12:00, and 14:00 and analysed for triglycerides, activated FVII (FVIIa), TF, FVIIa-antithrombin (FVIIa-AT), prothrombin fragment 1 + 2 (F1+2), and TF pathway inhibitor (TFPI). The gut bacteria composition, measured as gram-negative bacteria and diversity, was analysed in faecal samples. Results: Triglycerides, FVIIa, and FVIIa-AT increased significantly after high-fat meals, whereas F1 + 2 decreased equally and significantly over time after both meals. There were no significant changes in TF and TFPI over time. The postprandial changes in F1 + 2 and TFPI after high-fat meals were negatively correlated with diversity. Conclusions: Increased postprandial FVIIa is not accompanied by thrombin formation four hours after high-fat meals in patients with morbid obesity, possibly due to FVIIa-inhibition by AT.

Original languageEnglish
JournalThrombosis Research
Pages (from-to)260-267
Publication statusPublished - 1. Dec 2020


  • Blood samples
  • Coagulation activation
  • Endogenous thrombin formation
  • High-fat diet
  • Microbiota
  • Obesity
  • Tissue factor


Dive into the research topics of 'Postprandial factor VII activation does not increase plasma concentrations of prothrombin fragment 1 + 2 in patients with morbid obesity'. Together they form a unique fingerprint.

Cite this