This article reviews a study from Cell Metabolism, titled "Transketolase promotes MAFLD by limiting inosine-induced mitochondrial activity" [Tong L, Chen Z, Li Y, et al. Cell Metab. 2024, 36(5): 1013-1029.e5], and discusses its scientific implications. The study explores selective hepatic insulin resistance in metabolic dysfuction-associated fatty liver disease(MAFLD), where insulin stimulates lipid synthesis but not gluconeogenesis in resistant livers. It reveals the key role of transketolase(TKT) in MAFLD progression by disrupting pentose metabolism and nucleoside homeostasis, leading to inhibited mitochondrial activity. Targeting TKT with N-acetylgalactosamine-conjugated small interfering RNA(GalNAc-siTKT) improved metabolic dysfunction-associated steatohepatitis(MASH) and hepatic fibrosis.

This article reviews a study from Cell Metabolism, titled "Transketolase promotes MAFLD by limiting inosine-induced mitochondrial activity" [Tong L, Chen Z, Li Y, et al. Cell Metab. 2024, 36(5): 1013-1029.e5], and discusses its scientific implications. The study explores selective hepatic insulin resistance in metabolic dysfuction-associated fatty liver disease(MAFLD), where insulin stimulates lipid synthesis but not gluconeogenesis in resistant livers. It reveals the key role of transketolase(TKT) in MAFLD progression by disrupting pentose metabolism and nucleoside homeostasis, leading to inhibited mitochondrial activity. Targeting TKT with N-acetylgalactosamine-conjugated small interfering RNA(GalNAc-siTKT) improved metabolic dysfunction-associated steatohepatitis(MASH) and hepatic fibrosis.