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

Abstract

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 A 2 (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

Group X Secretory Phospholipase A2 Regulates Insulin Secretion through a Cyclooxygenase-2-dependent Mechanism

“…However, group IB sPLA 2 deficiency does not lead to alterations in basal or glucose-stimulated insulin secretion in mice (38) and group IIA sPLA 2 is naturally deficient in the inbred C57BL/6 mouse strain (39), ruling out a role for these two isozymes in the current study. We determined by real time RT-PCR that GV and GIID sPLA 2 mRNAs are expressed by MIN6 cells, whereas group III, group XIIA, and group XIIB mRNAs were not detected (data not shown).…”

Source and role of intestinally derived lysophosphatidic acid in dyslipidemia and atherosclerosis

“…One of the major pathways for the formation of LPA is through the action of autotaxin on LysoPC ( 23 ). A major source of intestinal LysoPC is through the action of PLA2G1B (45)(46)(47)(48)(49)(50). PLA2G1B is a pancreatic PLA 2 that hydrolyzes fatty acids at the sn -2 position of phospholipids in the lumen of the small intestine.…”

Analyses of Group III Secreted Phospholipase A2 Transgenic Mice Reveal Potential Participation of This Enzyme in Plasma Lipoprotein Modification, Macrophage Foam Cell Formation, and Atherosclerosis

“…Recent studies employing transgenic (Tg) (gain-of-function) and knock-out (loss-offunction) mice for several sPLA 2 s have revealed that individual enzymes exert distinct functions in vivo. Thus, PLA2G1B (group IB sPLA 2 ) plays a role in digestion of dietary phospholipids (3,4), PLA2G2A (group IIA sPLA 2 ) plays a role in antibacterial defense and possibly tumorigenesis (5)(6)(7)(8), PLA2G5 (group V sPLA 2 ) plays a role in zymosan-induced eicosanoid synthesis and phagocytosis by macrophages (9,10) and airway hypersensitivity (11), and PLA2G10 (group X sPLA 2 ) plays a role in allergen-induced asthma (12) and myocardial ischemia/ reperfusion injury (13). Thus far, beyond the well accepted regulatory role of group IVA cytosolic PLA 2 in arachidonate metabolism (14), PLA2G5 and PLA2G10 are the only two sPLA 2 s that have been proven to have the capacity to modulate arachidonic acid metabolism in vivo (15,16).…”