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      Relationship between free fatty acids, insulin resistance markers, and oxidized lipoproteins in myocardial infarction and acute left ventricular failure

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          Abstract

          Background

          The most common cause of myocardial infarction (MI) is stenotic atherosclerotic lesions in subepicardial coronary arteries. Artery disease progression induces clinical signs and symptoms, among which MI is the leader in mortality and morbidity. Recent studies have been trying to find new biochemical markers that could predict the evolution of clinical complications; among those markers, free fatty acids (FFA) and oxidative modification of low-density lipoproteins (oxidized LDL) have a special place.

          Materials and methods

          Seventy-nine ST-elevation MI patients were enrolled. The first group included MI patients without the signs of acute heart failure (Killip class I) while MI patients with Killip classes II–IV made up the second group. Thirty-three individuals with no cardiovascular disease were the controls. The lipid profile, serum oxidized LDL, and their antibodies, C-peptide and insulin were measured at days 1 and 12. The level of insulin resistance was assessed with the quantitative insulin sensitivity check index (QUICKI).

          Results

          MI patients had atherogenic dyslipidemia; however, the Killip II–IV group had the most pronounced and prolonged increase in FFA, oxidized LDL, and their antibodies. Additionally, positive correlations between FFA levels and creatine kinase activity (12 days, R = 0.301; P = 0.001) and negative correlations between the QUICKI index and FFA levels (R = −0.46; P = 0.0013 and R = −0.5; P = 0.01) were observed in the both groups.

          Conclusion

          The development of MI complications is accompanied by a significant increase in FFA levels, which not only demonstrate myocardial injury, but also take part in development of insulin resistance. Measuring FFA levels can have a great prognostic potential for risk stratification of both acute and recurrent coronary events and choice of treatment strategy.

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          Most cited references2

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          Acute elevation of NEFA causes hyperinsulinemia without effect on insulin secretion rate in healthy human subjects.

          Increased circulating levels of nonesterified free fatty acids (NEFA) have been observed in such hyperinsulinemic states as obesity, impaired glucose tolerance, diabetes, and dyslipidemia where they have been causally linked to the development of insulin resistance and hyperinsulinemia. The concentration of NEFA in plasma is believed to have direct modifying effects on insulin secretion and clearance. It remains controversial whether acute increases in NEFA potentiate insulin secretion in human subjects. We studied the effect of an acute elevation of NEFA during lipid-heparin infusion compared to a glycerol-only control on glucose-stimulated insulin secretion and clearance during a 120-min hyperglycemic (10 mM) clamp in 7 healthy normoglucose-tolerant volunteers. The metabolic clearance rate of C-peptide (MCR(CP)) was measured in each subject during the study by simultaneous infusion of C-peptide. Insulin secretion rate (ISR) was calculated from deconvolution of C-peptide data after correction for the rate of C-peptide infusion. Clearance rate of insulin (MCR(INS)) was calculated based upon endogenous ISR. Plasma glucose (mg/dL): basal (90-115 min) 90.2 +/- 2.8 vs. 90.2 +/- 2.3; clamp (150-240 min) 180.5 +/- 2.8 vs. 180.9 +/- 1.3. Plasma insulin (pmol/L): prebasal (fasting) 29.6 +/- 10.0 vs. 29.8 +/- 10.6; basal (90-115 min) 30.1 +/- 9.2 vs. 34.5 +/- 12.1; second phase clamp (210-240 min) 127.6 +/- 18.2 vs. 182.5 +/- 17.3*. Plasma NEFA (mM): prebasal 0.47 +/- 0.08 vs. 0.52 +/- 0.09; basal 0.35 +/- 0.05 vs. 0.98 +/- 0.02*; clamp (122-240 min) 0.06 +/- 0.02 vs. 0.77 +/- 0.06*. ISR (pmol/min): prebasal 72.7 +/- 7.5 vs. 72.0 +/- 7.9; second phase clamp (210-240 min) 268.5 +/- 27.2 vs. 200.2 +/- 23.7. MCR(INS) (mL/min): prebasal 3393 +/- 488 vs. 3370 +/- 511; clamp 2284 +/- 505 vs. 1214 +/- 153* (*p < 0.05 glycerol vs. intralipid/heparin). This study demonstrates that acute NEFA elevation causes hyperinsulinemia due to a significant decrease in systemic insulin clearance without increasing rates of insulin secretion.
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            The unstable atheroma

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              Author and article information

              Journal
              Diabetes Metab Syndr Obes
              Diabetes Metab Syndr Obes
              Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
              Dove Medical Press
              1178-7007
              2013
              18 February 2013
              : 6
              : 103-111
              Affiliations
              Federal State Budgetary Institution Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia
              Author notes
              Correspondence: EG Uchasova, FSBI Research Institute for Complex Issues of Cardiovascular Diseases SB RAMS, 6, Sosnovy Bvld Kemerovo 650002, Russian Federation, Tel +7 3842 64 05 53, Email evg.uchasova@ 123456yandex.ru
              Article
              dmso-6-103
              10.2147/DMSO.S37830
              3579407
              23550027
              668c59ac-d01c-4b04-bc3b-547d5f57cfa6
              © 2013 Gruzdeva et al, publisher and licensee Dove Medical Press Ltd.

              This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

              History
              Categories
              Original Research

              Endocrinology & Diabetes
              free fatty acids,insulin resistance,myocardial infarction
              Endocrinology & Diabetes
              free fatty acids, insulin resistance, myocardial infarction

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