scholarly journals Role of plasminogen activator inhibitor and free fatty acids in diagnosis of insulin resistance in patients with myocardial infarction

2011 ◽  
Vol 14 (4) ◽  
pp. 18-23 ◽  
Author(s):  
Olga Viktorovna Gruzdeva ◽  
Olga Leonidovna Barbarash ◽  
Olga Evgen'evna Akbasheva ◽  
Tatiana Sergeevna Fedorova ◽  
Elena Ivanovna Palicheva ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Early Recovery ◽  
C Peptide ◽  
Activator Inhibitor

Aim. Evaluation of the dynamics of the markers of insulin resistance in patients with myocardial infarction with ST-segment elevation with andwithout type 2 diabetes mellitus in the acute and early recovery period of the disease. Materials and methods. The study included 95 patients with myocardial infarction and 60 patients with myocardial infarction and type 2 diabetes.The control group consisted of 30 persons. We all studied at 1 st and 12 th day of myocardial infarction was determined by the content of free fattyacids, glucose, C-peptide, insulin in serum and plasminogen activator inhibitor in blood plasma. In addition, the 12 th day was determined postprandialglycemic, insulin and C-peptide 2h after a standard carbohydrate breakfast. Results. It is established that during myocardial infarction accompanied by the development of insulin resistance, characterized by postprandialglycemia and insulinemia, as well as the presence of elevated levels of free fatty acids, plasminogen activator inhibitor. Conclusion. The definition of metabolic markers of insulin resistance may be of great predictive capacity for assessing the risk of both acute coronaryevents and select tactics to further treatment

scholarly journals Role of plasminogen activator inhibitor and free fatty acids in diagnosis of insulin resistance in patients with myocardial infarction

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P5498-P5498 ◽  
Author(s):  
O. V. Gruzdeva ◽  
E. G. Uchasova ◽  
Y. A. Dyleva ◽  
E. V. Belik ◽  
E. A. Shurygina ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Activator Inhibitor

scholarly journals Free fatty acids enhance breast cancer cell migration through plasminogen activator inhibitor-1 and SMAD4

2009 ◽  
Vol 89 (11) ◽  
pp. 1221-1228 ◽  
Author(s):  
Chang Hyun Byon ◽  
Robert W Hardy ◽  
Changchun Ren ◽  
Selvarangan Ponnazhagan ◽  
Danny R Welch ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Fatty Acids ◽  
Cell Migration ◽  
Free Fatty Acids ◽  
Plasminogen Activator ◽  
Breast Cancer Cell ◽  
Plasminogen Activator Inhibitor ◽  
Cancer Cell Migration ◽  
Plasminogen Activator Inhibitor 1 ◽  
Activator Inhibitor

scholarly journals The Independence of Signaling Pathways Mediating Increased Expression of Plasminogen Activator Inhibitor Type1in HepG2 Cells Exposed to Free Fatty Acids or Triglycerides

2002 ◽  
Vol 3 (2) ◽  
pp. 109-118 ◽  
Author(s):  
Yabing Chen ◽  
David J. Schneider
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Plasminogen Activator ◽  
Hepg2 Cells ◽  
Plasminogen Activator Inhibitor ◽  
Fold Induction ◽  
Activator Inhibitor ◽  
Pai 1

We have shown that both free fatty acids (FFA) and triglycerides (TG) increase expression of plasminogen activator inhibitor type 1 (PAI-1) in vivo and in vitro. To determine signaling mechanisms responsible, HepG2 cells were exposed to FFA, emulsified TG, or the combination. The combination of FFA and TG increased PAI-1 to a greater extent than either agent alone (fold induction: 0.45mM FFA 1.7±0.2, 1000mg/dl TG 1.9±0.1, both 2.3±0.2, n=10, p<0.05 for comparison of combination with either alone). Cells transfected with PAI-1 5' flanking region containing the 4G or 5G polymorphism displayed similar activity in response to FFA, but modestly greater activity with the 4G polymorphism in response to TG (fold induction: 5G-1.28±0.14 and 4G- 1.46±0.13, n=6, p<0.05 for comparison). Deletion analyses demonstrated that FFA and TG induce PAI-1 expression through distinct regions of the promoter. Inhibition of protein kinase C inhibited the response to FFA but not TG. Accordingly, increased FFA and TG contribute to increased PAI- I through independent mechanisms.

scholarly journals Lipid, Adipokine аnd Ghrelin Concentrations in Myocardial Infarction Patients with Insulin Resistance

2013 ◽  
Vol 68 (7) ◽  
pp. 13-19 ◽  
Author(s):  
O. V. Gruzdeva ◽  
V. N. Karetnikova ◽  
O. Е. Akbasheva ◽  
T. S. Fedorova ◽  
E. V. Belik ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Significant Risk ◽  
Resistance Index ◽  
High Specificity ◽  
Early Recovery ◽  
Specificity And Sensitivity ◽  
History Of

Aim. The estimate insulin resistance in myocardial infarction. Patients and methods. The study involved 200 patients with myocardial infarction, in which on the 1st and 12th day of hospitalization measured glucose, insulin, insulin resistance index (IR), lipid profile, the concentration of adipokines and ghrelin. Results. IR was detected in 77% of patients and was associated with a history of factors of cardiovascular risk, adverse clinical course of the disease, lipid disorders. The most important marker was the level of free fatty acids. High risk associated with increased in 9 times the concentration of free fatty acids in blood plasma. Patients with IR observed increased concentrations of leptin, resistin, and reduced the protective effect of adiponectin. The high specificity and sensitivity characteristic of the concentration of ghrelin: its reduction by 4 times in the acute phase of myocardial infarction increases the risk of MI by 78%. Conclusions. Significant risk factors for MI myocardial infarction, along with insulinemia and glycemia, is to increase the concentration of free fatty acids and the disbalance in the system adipokines against deficiency of ghrelin in acute and early recovery periods of the disease. Free fatty acids and ghrelin are promising markers to stratify the risk of insulin resistance in patients with myocardial infarction. 

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