Long non-coding RNAs (lncRNAs) are important regulators of skeletal muscle physiology, with altered expression noted in several human diseases including type 2 diabetes. Here we report downregulation of TMEM9B-AS1, a previously uncharacterized lncRNA, in skeletal muscle of men with type 2 diabetes. We demonstrate that loss of TMEM9B-AS1 in primary human myotubes leads to reduction in protein synthesis, concomitant with reduced phosphorylation of ribosomal protein S6, downstream of ERK and mTOR pathways. Moreover, we show that TMEM9B-AS1 plays a pivotal role in the regulation of ribosomal biogenesis by facilitating mRNA stabilization of the transcription factor MYC through a direct physical interaction with the RNA-binding protein IGF2BP1. Disrupted ribosomal biogenesis resulting from downregulation of TMEM9B-AS1 links to the decrease in skeletal muscle mass observed in individuals with type 2 diabetes, shedding new light on the molecular mechanisms underlying this metabolic disorder.