scholarly journals Effect of individual dietary fatty acids on postprandial activation of blood coagulation factor VII and fibrinolysis in healthy young men

2003 ◽  
Vol 77 (5) ◽  
pp. 1125-1132 ◽  
Author(s):  
Tine Tholstrup ◽  
George J Miller ◽  
Anette Bysted ◽  
Brittmarie Sandström
Keyword(s):  
Fatty Acids ◽  
Blood Coagulation ◽  
Young Men ◽  
Coagulation Factor ◽  
Dietary Fatty Acids ◽  
Factor Vii ◽  
Coagulation Factor Vii

scholarly journals Circulating Tissue Factor Procoagulant Activity and Thrombin Generation in Patients with Type 2 Diabetes: Effects of Insulin and Glucose

2007 ◽  
Vol 92 (11) ◽  
pp. 4352-4358 ◽  
Author(s):  
Guenther Boden ◽  
Vijender R. Vaidyula ◽  
Carol Homko ◽  
Peter Cheung ◽  
A. Koneti Rao
Keyword(s):  
Type 2 Diabetes ◽  
Tissue Factor ◽  
Blood Coagulation ◽  
Coagulation Factor ◽  
Procoagulant Activity ◽  
Factor Vii ◽  
Coagulation Factor Vii ◽  
Glucose Levels ◽  
Study Protocols

Abstract Context: Type 2 diabetes mellitus (T2DM) is a hypercoagulable state. Tissue factor (TF) is the principal initiator of blood coagulation. Objective: Our objective was to examine the effects of hyperglycemia and hyperinsulinemia on the TF pathway of blood coagulation in T2DM. Design: Three study protocols were used: 1) acute correction of hyperglycemia (with iv insulin) followed by 24 h of euglycemia, 2) 24 h of selective hyperinsulinemia, and 3) 24 h of combined hyperinsulinemia and hyperglycemia. Setting: The study took place at a clinical research center. Study Participants: Participants included 18 T2DM patients and 22 nondiabetic controls. Results: Basal TF-procoagulant activity (TF-PCA), monocyte TF mRNA, plasma coagulation factor VII (FVIIc), and thrombin-anti-thrombin complexes were higher in T2DM than in nondiabetic controls, indicating a chronic procoagulant state. Acutely normalizing hyperglycemia over 2–4 h resulted in a small (∼7%) but significant decline in TF-PCA with no further decline over 24 h. Raising insulin levels alone raised TF-PCA by 30%, whereas raising insulin and glucose levels together increased TF-PCA (by 80%), thrombin-anti-thrombin complexes, and prothrombin fragment 1.2. Plasma FVIIa and FVIIc declined with increases in TF-PCA. Conclusion: We conclude that the combination of hyperglycemia and hyperinsulinemia, common in poorly controlled patients with T2DM, contributes to a procoagulant state that may predispose these patients to acute cardiovascular events.

scholarly journals Effects of dietary fat quantity and composition on fasting and postprandial levels of coagulation factor VII and serum choline-containing phospholipids

2003 ◽  
Vol 90 (2) ◽  
pp. 329-336 ◽  
Author(s):  
Anja Schou Lindman ◽  
Hanne Müller ◽  
Ingebjørg Seljeflot ◽  
Hans Prydz ◽  
Marit Veierød ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
Coagulation Factor ◽  
Factor Vii ◽  
High Fat ◽  
Coagulation Factor Vii ◽  
Low Fat Diet

Dietary fat influences plasma levels of coagulation factor VII (FVII) and serum phospholipids (PL). It is, however, unknown if the fat-mediated changes in FVII are linked to PL. The present study aimed to investigate the effects of dietary fat on fasting and postprandial levels of activated FVII (FVIIa), FVII coagulant activity (FVIIc), FVII protein (FVIIag) and choline-containing PL (PC). In a randomized single-blinded crossover-designed study a high-fat diet (HSAFA), a low-fat diet (LSAFA), both rich in saturated fatty acids, and a high-fat diet rich in unsaturated fatty acids (HUFA) were consumed for 3 weeks. Twenty-five healthy females, in which postprandial responses were studied in a subset of twelve, were included. The HSAFA diet resulted in higher levels of fasting FVIIa and PC compared with the LSAFA and the HUFA diets (all comparisonsP≤0·01). The fasting PC levels after the LSAFA diet were also higher than after the HUFA diet (P<0·001). Postprandial levels of FVIIa and PC were highest on the HSAFA diet and different from LSAFA and HUFA (all comparisonsP≤0·05). Postprandial FVIIa was higher on the HUFA compared with the LSAFA diet (P<0·03), whereas the HUFA diet resulted in lower postprandial levels of PC than the LSAFA diet (P<0·001). Significant correlations between fasting levels of PC and FVIIc were found on all diets, whereas FVIIag was correlated to PC on the HSAFA and HUFA diet. The present results indicate that dietary fat, both quality and quantity, influences fasting and postprandial levels of FVIIa and PC. Although significant associations between fasting FVII and PC levels were found, our results do not support the assumption that postprandial FVII activation is linked to serum PC.

scholarly journals Coagulation Factor VII Mass and Activity in Young Men With Myocardial Infarction at a Young Age

1995 ◽  
Vol 15 (5) ◽  
pp. 655-664 ◽  
Author(s):  
Elisabeth Moor ◽  
Angela Silveira ◽  
Ferdinand van’t Hooft ◽  
Anna Maija Suontaka ◽  
Per Eriksson ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Young Men ◽  
Coagulation Factor ◽  
Young Age ◽  
Factor Vii ◽  
Coagulation Factor Vii

Do oxidized fatty acids activate coagulation factor VII during post-prandial lipemia in women?

2003 ◽  
Vol 89 (04) ◽  
pp. 654-659 ◽  
Author(s):  
Robert Wilson ◽  
Karin Lyall ◽  
Margaret Millar ◽  
Louise Smyth ◽  
Claire Pearson ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Body Weight ◽  
Edible Oils ◽  
Plasma Lipid ◽  
Coagulation Factor ◽  
Factor Vii ◽  
Gas Chromatography Mass Spectrometry ◽  
Walnut Oil ◽  
Plasma Triglycerides ◽  
Coagulation Factor Vii

SummaryFactor VII is activated to VIIa within hours after dietary fat, irrespective of its fatty acid composition. Edible oils contain oxidized material (hydroxy fatty acids, HOFA). Twenty-five fasting women, aged 38 (10) years, consumed 30 g walnut oil containing 26 (6) mg HOFA. Blood was collected 2-hourly to measure plasma triglycerides and plasma lipid HOFA by gas chromatography/mass spectrometry. VII and sTF-dependent VIIa were quantified at 0, 6 and 24 h. Increased plasma triglycerides and HOFA (areas under the-curve 0-8 h, AUC) were related r = 0.83, p <0.001. VIIa increased from 2.6 (1.4) to 4.2 (1.9) ng/mL at 6 h (p <0.001). Plasma VII remained constant. VIIa (6 h) was related to plasma triglycerides- and HOFA-AUC: r = 0.38 and 0.53, respectively (both p <0.05). Plasma VIIa was also related to body weight, fasting triglycerides, HOFA and VII. Only HOFA-AUC and body weight related to VIIa (6 h) in stepwise regression analysis (p = 0.007 and 0.038, respectively). Oxidized, not normal, fat activates VII and could increase coronary risk in humans.

scholarly journals Postprandial coagulation factor VII activity: the effect of monounsaturated fatty acids

1997 ◽  
Vol 77 (4) ◽  
pp. 537-549 ◽  
Author(s):  
Helen M. Roche ◽  
Michael J. Gibney
Keyword(s):  
Fatty Acids ◽  
Regression Analysis ◽  
Plasma Lipid ◽  
Area Under The Curve ◽  
Coagulation Factor ◽  
Random Order ◽  
Monounsaturated Fatty Acids ◽  
Factor Vii ◽  
Activity Levels ◽  
Coagulation Factor Vii

The present study investigated the effect of monounsaturated fatty acids (MUFA) on postprandial coagulation factor VII activity. Fifteen healthy male volunteers consumed three meals containing equal amounts (40g) of fat, but providing different proportions of MUFA (12,17 and 24% energy)in random order. Fasting and postprandial blood samples were drawn every hour for 9 h. The magnitude of the postprandial triacylglycerolaemic response and the postprandial plasma nonesterifled fatty acid (NEFA) concentrations were not significantly different following the three meals. Coagulation factor VII was activated during postprandial triacylglycerolaemia but the area under the curve of postprandial coagulation factor VII activity was not significantly different following the three meals. Regression analysis showed that fasting factor VII activity was the single mast important factor affecting postprandial factor VII activity, irrespective of plasma lipid concentrations and meal fat composition. Peak postprandial factor VII activity was attained significantly earlier following the high-MUFA meal compared with the low-MUFA meal (6·33 (SD 2·16) h, 3·60 (SD 1·81)h respectively; P = 0·016). Regression analysis showed that meal MUFA content was the primary determinant of time to peak postprandial factor VII activity. Although the magnitude of postprandial coagulation factor VII activity was not affected by meal MUFA content, peak postprandial factor VII activity occurred earlier and fasting activity levels were quickly restored following the high-MUFA meal. A short-lived increase in factor VII activity may be more beneficial than a prolonged thrombotic response.

scholarly journals Characterization of Transcriptional Regulatory Elements in the Promoter Region of the Murine Blood Coagulation Factor VII Gene

1998 ◽  
Vol 273 (4) ◽  
pp. 2277-2287 ◽  
Author(s):  
Daniel R. Stauffer ◽  
Beatrice N. Chukwumezie ◽  
Julie A. Wilberding ◽  
Elliot D. Rosen ◽  
Francis J. Castellino
Keyword(s):  
Blood Coagulation ◽  
Promoter Region ◽  
Coagulation Factor ◽  
Regulatory Elements ◽  
Factor Vii ◽  
Transcriptional Regulatory Elements ◽  
Coagulation Factor Vii ◽  
Transcriptional Regulatory

The Effect of O-Fucosylation on the First EGF-like Domain from Human Blood Coagulation Factor VII†

Biochemistry ◽  
1999 ◽  
Vol 38 (22) ◽  
pp. 7097-7110 ◽  
Author(s):  
Yung-Hsiang Kao ◽  
Geoffrey F. Lee ◽  
Yang Wang ◽  
Melissa A. Starovasnik ◽  
Robert F. Kelley ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Human Blood ◽  
Coagulation Factor ◽  
Factor Vii ◽  
Coagulation Factor Vii ◽  
Human Blood Coagulation

scholarly journals A candidate activation pathway for coagulation factor VII

2019 ◽  
Vol 476 (19) ◽  
pp. 2909-2926
Author(s):  
Tina M. Misenheimer ◽  
Kraig T. Kumfer ◽  
Barbara E. Bates ◽  
Emily R. Nettesheim ◽  
Bradford S. Schwartz
Keyword(s):  
Tissue Factor ◽  
Blood Coagulation ◽  
Factor Viia ◽  
Coagulation Factor ◽  
Factor Ix ◽  
Factor Vii ◽  
Factor X ◽  
Contact Activation ◽  
Coagulation Factor Vii ◽  
Factor Viiia

Abstract The mechanism of generation of factor VIIa, considered the initiating protease in the tissue factor-initiated extrinsic limb of blood coagulation, is obscure. Decreased levels of plasma VIIa in individuals with congenital factor IX deficiency suggest that generation of VIIa is dependent on an activation product of factor IX. Factor VIIa activates IX to IXa by a two-step removal of the activation peptide with cleavages occurring after R191 and R226. Factor IXaα, however, is IX cleaved only after R226, and not after R191. We tested the hypothesis that IXaα activates VII with mutant IX that could be cleaved only at R226 and thus generate only IXaα upon activation. Factor IXaα demonstrated 1.6% the coagulant activity of IXa in a contact activation-based assay of the intrinsic activation limb and was less efficient than IXa at activating factor X in the presence of factor VIIIa. However, IXaα and IXa had indistinguishable amidolytic activity, and, strikingly, both catalyzed the cleavage required to convert VII to VIIa with indistinguishable kinetic parameters that were augmented by phospholipids, but not by factor VIIIa or tissue factor. We propose that IXa and IXaα participate in a pathway of reciprocal activation of VII and IX that does not require a protein cofactor. Since both VIIa and activated IX are equally plausible as the initiating protease for the extrinsic limb of blood coagulation, it might be appropriate to illustrate this key step of hemostasis as currently being unknown.

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