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Background: Insulin resistance (IR) is known to be characteristic of type 2 diabetes mellitus, and is regarded as an important mechanism in disease pathogenesis. One of the key pathogenetic mechanisms of IR progression is impaired free fatty acid (FFA) metabolism. Plasminogen-activator inhibitor 1 (PAI-1) and key inflammation markers, ie, interleukin 6 (IL-6) and C-reactive protein (CRP), also play a role.
Purpose: To assess the changing levels of the metabolic proinflammation IR markers IL-6, CRP and PAI-1 and their association with the presence or absence of type 2 diabetes mellitus in myocardial infarction (MI) patients during their hospital stay.
Methods: The patients were divided into two groups: group 1 included 95 nondiabetic MI patients, and group 2 enrolled 40 diabetic MI patients. The control group consisted of 30 sex- and age-matched volunteers. Serum IL-6 and CRP levels as well as FFA, glucose, C-peptide, insulin, and plasma PAI-1 concentrations were measured at days 1 and 12 from MI onset.
Results: At day 1, there was an increase in glucose concentrations, which remained high in both groups by day 12 but was much higher in the diabetic patients. Basal insulin and C-peptide levels did not differ significantly from those in the control group. The quantitative insulin sensitivity-check index in both groups was significantly different from that in controls. FFA concentrations at day 1 in both diabetic and nondiabetic patients increased; by day 12, they had decreased but were still higher than the controls. CRP and IL-6 levels at day 1 were higher in all the patients, but diabetic patients had the highest levels; by day 12, the levels were lower but still 2.4-fold (IL-6) and 12.5-fold (CRP) higher than those in the control group.
Conclusion: This study showed that MI is accompanied both by activated inflammatory response and IR. Strong correlations between IL-6 and FFA concentrations demonstrate that nonspecific inflammation factors are involved in IR development in MI patients. Consequently, these inflammatory cytokines might cause the development of IR.
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