ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2013
Plasminogen activator inhibitor-1, free fatty acids, and insulin resistance in patients with myocardial infarction.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Review
- Effect of Glucose Levels on Cardiovascular Risk.Cells · 2022Review
- Brown adipose tissue prevents glucose intolerance and cardiac remodeling in high-fat-fed mice after a mild myocardial infarction.International journal of obesity (2005) · 2022Article
- MIKB: A manually curated and comprehensive knowledge base for myocardial infarction.Computational and structural biotechnology journal · 2021Article
- Relationship key factor of inflammation and the development of complications in the late period of myocardial infarction in patients with visceral obesity.BMC cardiovascular disorders · 2017Article
- Correlation between serum free fatty acids levels and Gensini score in elderly patients with coronary heart disease.Journal of geriatric cardiology : JGC · 2014Article
- Serum adiponectin level in diabetic patients with and without Helicobacter pylori infection: is there any difference?TheScientificWorldJournal · 2014Article
- Serum levels of thrombotic markers in patients with acute myocardial infarction.International journal of clinical and experimental medicine · 2014Article
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Authors and funding
6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundInsulin resistance is known to be a common feature of type 2 diabetes mellitus and is regarded as an important mechanism in the pathogenesis of this disease. The key pathogenetic mechanisms of insulin resistance progression are free fatty acids metabolism impairment and enhanced activity of plasminogen activator inhibitor 1. Both free fatty acids and plasminogen activator inhibitor 1 are recognized as risk factors for coronary heart disease.
methodsTHE PATIENTS WERE DIVIDED INTO TWO GROUPS: group 1 included 65 non-diabetic myocardial infarction patients and group 2 enrolled 60 diabetic myocardial infarction patients. The control group consisted of 30 sex- and age-matched volunteers. The concentration of serum free fatty acids, glucose, C-peptide, and insulin were measured on the 1st and 12th days of the study. All the patients had their postprandial glycemia, insulin, and C-peptide concentrations measured 2 hours after a standard carbohydrate breakfast containing 360 kcal (protein 20 g, carbohydrate 57 g, and fat 9 g).
resultsFree fatty acids levels in group 1 and in group 2 exceeded the control group values by 7-fold and 11-fold, respectively. Plasminogen activator inhibitor 1 concentration was 2.5-fold higher in group 1 and 4.6-fold higher in group 2 compared to the control group on the 1st day from the myocardial infarction onset. In addition, plasminogen activator inhibitor 1 concentration was significantly reduced in both groups on the 12th day from the myocardial infarction onset; however, it did not achieve the control group values.
conclusionIncreased postprandial glucose level, insulinemia, and elevated levels of free fatty acids and plasminogen activator inhibitor are associated with myocardial infarction-associated progression of insulin resistance. However, insulin resistance metabolic markers are of great predictive capacity in the assessment of risk of acute coronary events.
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