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The enhanced hepatic mitochondrial activity in the context of TKT deficiency has been shown to be the result of increased phospholipid synthesis, particularly increased synthesis of phosphatidylcholine which represents the major phospholipid in the mitochondrial membrane

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212 Further, increased expression and low methylation of CDKN1A and PDE7B genes in T2DM can lead to impaired insulin release that is stimulated by glucose in T2DM patients