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While these findings suggest increased hepatic de novo gluconeogenesis, the gluconeogenic response of NKCC2A KO mice to exogenous pyruvate, which is converted into glucose in the liver, kidneys and small intestines (Stumvoll et al., 1998

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Transplanting bone marrow from these trained mice into normal-diet recipients enlarges atherosclerotic lesions (103, 104)

Coupling global methylation and gene expression profiles reveal key pathophysiological events in liver injury induced by a methyl-deficient diet