High Plasma Phospholipase A 2 Activity, Inflammation Markers, and LDL Alterations in Obesity With or Without Type 2 Diabetes

• Published in: Obesity (Silver Spring, Md.) Md.), 2012-09, Vol.18 (10), p.2023-2029
• Main Authors: Garces, Fatima, López, Flor, Niño, Cladimar, Fernandez, Anazita, Chacin, Luis, Hurt‐Camejo, Eva, Camejo, Germán, Apitz‐Castro, Rafael
• Format: Article
• Language: English
• ISSN: 1930-7381; 1930-739X
• DOI: 10.1038/oby.2010.9

Plasma phospholipases A 2 (PLA 2 ) hydrolyze phospholipids of circulating lipoproteins or deposited in arteries producing bioactive lipids believed to contribute to the atherosclerotic inflammatory response. PLA 2 (s) are elevated in obesity and type 2 diabetes (T2D) but it is not clear which of these conditions is the cause since they frequently coexist. This study attempts to evaluate if high plasma PLA 2 (s) activities and markers of their effects in lipoproteins are associated with obesity or T2D diabetes, or with both. Total PLA 2 and Ca 2+ ‐dependent and ‐independent activities, lipids, lipoproteins, apoAI, and apoB apolipoproteins and affinity of apoB‐lipoproteins for arterial proteoglycans were measured, as well as Inflammation markers. These parameters were evaluated in plasma samples of four groups: (i) apparently healthy controls with normal BMI (nBMI), (ii) obese subjects with no T2D, (iii) patients with T2D but with nBMI, and (iv) obese patients with T2D. PLA 2 activities were measured in the presence and absence of Ca 2+ and in the presence of specific inhibitors. Obese subjects, with or without T2D, had high activities of total PLA 2 and of Ca 2+ ‐dependent and Ca 2+ ‐independent enzymes. The activities were correlated with inflammation markers in obese subjects with and without diabetes and with alterations of low‐density lipoproteins (LDLs) that increased their affinity for arterial proteoglycans. Ca 2+ ‐dependent secretory (sPLA 2 ) enzymes were the main responsible of the obesity‐associated high activity. We speculate that augmented PLA 2 (s) activity that increases affinity of circulating LDL for arterial intima proteoglycans could be another atherogenic component of obesity.