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Phospholipase A2 enzymes in metabolic and cardiovascular diseases

Hui, David Y.

Current Opinion in Lipidology: June 2012 - Volume 23 - Issue 3 - p 235–240
doi: 10.1097/MOL.0b013e328351b439
LIPID METABOLISM: Edited by Jeffrey S. Cohn

Purpose of review The phospholipase A2 (PLA2) family of proteins includes lipolytic enzymes that liberate the sn-2 fatty acyl chains from phospholipids to yield nonesterified fatty acids and lysophospholipids. The purpose of this review is to discuss recent findings showing distinct roles of several of these PLA2 enzymes in inflammatory metabolic diseases such as diabetes and atherosclerosis.

Recent findings The group 1B PLA2 digestion of phospholipids in the intestinal lumen facilitates postprandial lysophospholipid absorption, which suppresses hepatic fatty acid oxidation leading to increased VLDL synthesis, decreased glucose tolerance, and promotion of tissue lipid deposition to accentuate diet-induced hyperlipidemia, diabetes, and obesity. Other secretory PLA2s promote inflammatory metabolic diseases by generating bioactive lipid metabolites to induce inflammatory cytokine production, whereas the major intracellular PLA2s, cPLA2α, and iPLA2, generate arachidonic acid and lysophosphatic acid in response to extracellular stimuli to activate leukocyte chemotactic response.

Summary Each member of the PLA2 family of enzymes serves a distinct role in generating active lipid metabolites that promote inflammatory metabolic diseases including atherosclerosis, hyperlipidemia, obesity, and diabetes. The development of specific drugs that target one or more of these PLA2 enzymes may be novel strategies for treatment of these chronic inflammatory metabolic disorders.

Department of Pathology, Metabolic Diseases Institute, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA

Correspondence to David Y. Hui, PhD, Department of Pathology (ML 0507), Metabolic Diseases Institute, University of Cincinnati College of Medicine, 2120 E. Galbraith Road, Cincinnati, OH 45237-0507, USA. Tel: +1 513 558 9152; fax: +1 513 558 1312; e-mail:

© 2012 Lippincott Williams & Wilkins, Inc.