Insulin resistance and inflammation markers in myocardial infarction

Abstract

BackgroundInsulin 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.PurposeTo 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.MethodsThe 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.ResultsAt 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.ConclusionThis 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.