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Background  Skeletal muscle has an important role in regulating whole-body energy homeostasis, and energy production depends on the efficient function of mitochondria. We demonstrated previously that AT-rich interactive domain 5b ( Arid5b ) knockout ( Arid5b   −/−  ) mice were lean and resistant to high-fat diet (HFD)-induced obesity. While a potential role of  Arid5b  in energy metabolism has been suggested in adipocytes and hepatocytes, the role of  Arid5b  in skeletal muscle metabolism has not been studied. Therefore, we investigated whether energy metabolism is altered in  Arid5b   −/−   skeletal muscle.    Results   Arid5b   −/−   skeletal muscles showed increased basal glucose uptake, glycogen content, glucose oxidation and ATP content. Additionally, glucose clearance and oxygen consumption were upregulated in  Arid5b   −/−   mice. The expression of glucose transporter 1 (GLUT1) and 4 (GLUT4) in the gastrocnemius (GC) muscle remained unchanged. Intriguingly, the expression of TBC domain family member 1 (TBC1D1), which negatively regulates GLUT4 translocation to the plasma membrane, was suppressed in  Arid5b   −/−   skeletal muscle. Coimmunofluorescence staining of the GC muscle sections for GLUT4 and dystrophin revealed increased GLUT4 localization at the plasma membrane in  Arid5b   −/−   muscle.    Conclusions  The current study showed that the knockout of  Arid5b  enhanced glucose metabolism through the downregulation of TBC1D1 and increased GLUT4 membrane translocation in skeletal muscle.    Electronic supplementary material  The online version of this article (10.1186/s40659-020-00313-3) contains supplementary material, which is available to authorized users.

Increased glucose metabolism in Arid5b−/− skeletal muscle is associated with the down-regulation of TBC1 domain family member 1 (TBC1D1)