Though γ-aminobutyric acid (GABA) serves as the primary inhibitory neurotransmitter in the brain, its numerous biological activities in the periphery, including anti-inflammatory and antidiabetic functions, have been documented. In addition, GABA may be a mediator underlying effects of ketone bodies/ketogenic diets on muscle regeneration. Here, we investigated the effects of GABA on muscle regeneration in type 1 diabetes mouse models. Akita and wild-type (WT) mice were treated with GABA in drinking water for 6 wk, followed by cardiotoxin (CTX)-induced muscle injury. At 5 days postinjury, GABA treatment exhibited no effects on regenerating myofiber size in both WT and Akita mice. Unexpectedly, regenerating GABA-treated Akita muscles exhibited significantly increased embryonic myosin heavy chain (eMHC) expression and higher intramuscular macrophage content, suggesting delays in muscle regeneration and in elevated macrophage infiltration in diabetic muscles. Next, we determined if GABA treatment delayed the inflammatory process during muscle regeneration. Providing GABA in the drinking water during the peak inflammatory period (