Complementary hyperpolarized 13C and 15N MRI reveal divergent signatures of hepatic injury and methyl-donor metabolism

-dimethylglycine as a readout of hepatic one-carbon metabolism over a multi-minute timescale. While malate signal increased markedly in steatohepatitis, dimethylglycine formation was reduced despite comparable parent betaine signal, indicating impaired metabolic engagement rather than altered substrate delivery. These hyperpolarized contrast mechanisms provide complementary metabolic readouts of hepatic injury and methyl-donor metabolism in vivo, extending hyperpolarized MRI toward probing endogenous metabolic processes on extended timescales.