The phospholipase A2 family's role in metabolic diseases: Focus on skeletal muscle

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

The prevalence of obesity and type 2 diabetes has increased substantially in recent years creating a global health burden. In obesity, skeletal muscle, the main tissue responsible for insulin-mediated glucose uptake, exhibits dysregulation of insulin signaling, glucose uptake, lipid metabolism, and mitochondrial function, thus, promoting type 2 diabetes. The phospholipase A2 (PLA2) enzyme family mediates lipid signaling and membrane remodeling and may play an important role in metabolic disorders such as obesity, diabetes, hyperlipidemia, and fatty liver disease. The PLA2 family consists of 16 members clustered in four groups. PLA2s hydrolyze the sn-2 ester bond of phospholipids generating free fatty acids and lysophospholipids. Differential tissue and subcellular PLA2 expression patterns and the abundance of distinct fatty acyl groups in the target phospholipid determine the impact of individual family members on metabolic functions and, potentially, diseases. Here, we update the current knowledge of the role of the PLA2 family in skeletal muscle, with a view to their potential for therapeutic targeting in metabolic diseases.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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