Type 1 diabetes, or T1D, is an autoimmune disease in which the body’s immune cells — led by inflammatory macrophages — attack and destroy the beta cells of the pancreas that produce insulin.
Researchers have long tried to unravel the signaling that provokes this attack. One of the less-studied forms of signaling is inflammatory lipids.
In a study published in JCI Insight, Sasanka Ramanadham, Ph.D., and colleagues at the University of Alabama at Birmingham, at other universities in the United States and in Greece have identified a proinflammatory lipid profile that precedes development of T1D in a mouse model and in children under the age 15 who are at high risk for T1D.
This finding may identify candidate lipid therapeutic targets to prevent T1D.
Phospholipase A2, or PLA2, enzymes can release a free fatty acid from glycerophospholipids. When the free fatty acid is arachidonic acid, it can be metabolized by several other enzyme classes to produce oxidized bioactive lipids, including some potent inflammatory eicosanoids.
One of the phospholipase A2 enzymes is a calcium-independent phospholipase A2, designated iPLA2-beta. Its activation promotes poor outcomes in experimental and clinical diabetes.
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