LPCAT3 and Glucose intolerance: These changes coincided with the association between circulating insulin and the expression of LPCAT3, an enzyme involved in the transacylation of LPC to synthesize PC (a part of Lands’ cycle), in skeletal muscle that was reported in animal-level experiment studies: the knockout of LPCAT3 mediated LPC accumulation in muscle and improved insulin sensitivity under a high-fat diet, while the overexpression of LPCAT3 in skeletal muscle exhibited decreased LPC in muscle cells and promoted glucose intolerance [11].