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Group 1B Phospholipase A₂–Mediated Lysophospholipid Absorption Directly Contributes to Postprandial Hyperglycemia

Department of Pathology, Genome Research Institute, University of Cincinnati, Cincinnati, Ohio

Address correspondence and reprint requests to David Y. Hui, Department of Pathology (ML 0507), Genome Research Institute, University of Cincinnati, 2120 E. Galbraith Rd., Cincinnati, OH 45237-0507. E-mail: huidy{at}email.uc.edu

Abbreviations: G6Pase, glucose-6-phosphatase; JNK, c-Jun NH₂-terminal kinase; LPC, lysophosphatidylcholine; PKC-, protein kinase C-; Pla2g1b, group 1B phospholipase A₂

Postprandial hyperglycemia is an early indicator of abnormality in glucose metabolism leading to type 2 diabetes. However, mechanisms that contribute to postprandial hyperglycemia have not been identified. This study showed that mice with targeted inactivation of the group 1B phospholipase A₂ (Pla2g1b) gene displayed lower postprandial glycemia than that observed in wild-type mice after being fed a glucose-rich meal. The difference was caused by enhanced postprandial glucose uptake by the liver, heart, and muscle tissues as well as altered postprandial hepatic glucose metabolism in the Pla2g1b^–/– mice. These differences were attributed to a fivefold decrease in the amount of dietary phospholipids absorbed as lysophospholipids in Pla2g1b^–/– mice compared with that observed in Pla2g1b^+/+ mice. Elevating plasma lysophospholipid levels in Pla2g1b^–/– mice via intraperitoneal injection resulted in glucose intolerance similar to that exhibited by Pla2g1b^+/+ mice. Studies with cultured hepatoma cells revealed that lysophospholipids dose-dependently suppressed insulin-stimulated glycogen synthesis. These results demonstrated that reduction of lysophospholipid absorption enhances insulin-mediated glucose metabolism and is protective against postprandial hyperglycemia.

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