FEEDING AWAY INFLAMMATION – CONJUGATED LINOLEIC ACIDS DECREASE PANCREATIC PHOSPHOLIPASE A2 ACTIVITY*

ABSTRACT

Conjugated linoleic acids (CLAs) are positional and geometric isomers of linoleic acid derived from food, mainly from milk and meat products. CLAs are ligands of peroxisome proliferator-activated gamma receptors. Phospholipases A₂ (PLA₂) represent a diverse group of enzymes that catalyze the hydrolysis of ester bonds at the sn-2 position of membrane phospholipids and release fatty acids and lysophospholipids. The objective of the study was to answer the question whether the release of linoleic acid by pancreatic PLA₂ may change in the CLA-containing environment. In this study, linoleic acid released by pancreatic PLA₂ was a substrate for purified lipoxygenase – an enzyme converting it into hydroxylated derivatives including 9- and 13-hydroxyoctadecadienoic acid (9-,13-HODE). In this method, the activity of PLA₂ was determined by high-performance liquid chromatography. In vitro incubation of hog PLA₂ with CLA contributed to a noticeable fall in the synthesis of HODEs (P = 0.003; Kruskal–Wallis test). The concentration of HODEs decreased by 40.2% (for the cis-9, trans-11 CLA isomer; P = 0.007, Mann–Whitney test, n = 5) and by 27% (for the trans-10, cis-12 CLA isomer; P = 0.007, Mann–Whitney test, n = 5) as compared with the control (enzyme incubated without CLA). The inhibition exerted by cis-9, trans-11 CLA isomer was significantly greater than that by trans-10, cis-12 CLA isomer (P = 0.032, Mann–Whitney test, n = 5).

PRACTICAL APPLICATIONS

This study is an attempt to clarify the response to the question whether some food ingredients such as conjugated linoleic acid (CLA) may be useful as an agent supporting the treatment of gastrointestinal disorders. It was observed under in vitro conditions that CLA isomers inhibited the phosphatidylcholine hydrolysis. By using purified enzymes, CLA was shown to contribute to local reduction of availability of linoleic acid and its metabolites (9- and 13-hydroxyoctadecadienoic acid) through inhibition of phospholipid hydrolysis.