Relationship between polyunsaturated fatty acid composition in serum phospholipids, systemic low-grade inflammation, and glycemic control in patients with type 2 diabetes and atherosclerotic cardiovascular disease

BACKGROUND: There are inconsistent data about the role of serum phospholipid fatty acid composition in patients with type 2 diabetes (T2DM) and atherosclerotic cardiovascular disease (ASCVD). The aim of the study was to investigate the relationship between serum phospholipid fatty acid composition, systemic low-grade inflammation, and glycemic control in high-risk T2DM patients. METHODS: Seventy-four patients (26% women, mean age 65.6 ± 6.8 years) with T2DM (median diabetes duration 10 years) and documented ASCVD (74 with coronary artery disease, 26 with peripheral arterial disease) were enrolled in the study. Baseline HbA(1c) was estimated using turbidimetric inhibition immunoassay. According to the median value of HbA(1c) the patients were grouped into those with HbA(1c) < 7.0% (< 53 mmol/mol) (n = 38) and those with HbA(1c) ≥ 7.0% (≥ 53 mmol/mol) (n = 36). Serum phospholipid fatty acids were measured with gas chromatography. RESULTS: Patients with HbA(1c) ≥ 7.0%, compared with those with HbA(1c) < 7.0% had similar composition of saturated and monounsaturated fatty acids in serum phospholipids, but had higher concentrations of linoleic acid (LA) and higher n-6/n-3 polyunsaturated fatty acid (PUFA) ratio as well as lower levels of eicosapentaenoic acid (EPA), total n-3 PUFAs, and the EPA/arachidonic acid ratio. We found that LA (r = 0.25; p = 0.03) and n-6/n-3 PUFA ratio (r = 0.28; p = 0.02) were positively correlated with HbA(1c). Multivariate logistic regression analysis showed that n-6/n-3 PUFA ratio, hsCRP and T2DM duration were independent predictors of worse glycemic control in patients with T2DM and ASCVD. CONCLUSIONS: This study showed that glycemic control in high-risk T2DM patients with ASCVD was significantly associated with unfavorable serum phospholipid n-6/n-3 PUFA ratio and greater systemic inflammation.