We aimed to determine facial and hind paw allodynia in diabetic neuropathy model induced by streptozotocin (STZ) treatment and to determine the anti-allodynic effect of metformin treatment. STZ was intraperitoneally injected (150 mg/kg) to induce painful diabetic neuropathy, and 200 mg/kg of metformin was injected intraperitoneally on the 21st day. Both of the mechanical and cold sensitivity in facial and paw withdrawal region were quantified using von-Frey filaments and acetone solution, respectively. To test heat hyperalgesia, mice were placed into a plastic chamber with a glass floor and radiant heat was applied to the plantar surface of the hind paw. The changes of AMPK or mTOR and related proteins, p-p38 MAPK, glia in TG and TNC were examined using western blot or immunohistochemistry. Mice showed significant mechanical allodynia in facial and hind paw 3 weeks after STZ injection. In contrast, STZ administration did not increase facial or hind paw responses to cold and heat stimuli. The mechanical allodynia was significantly reduced in both facial and hind paw 2 hour after metformin administration. In TG tissue, STZ and metformin-treated mice only altered p-AMPK and p-mTOR expression. In TNC tissue, metformin treatment did not reduce the increased expression of GFAP and Iba-1, whereas it significantly reduced the increased expression of p-p38 in STZ mice. These findings demonstrated that metformin treatment reduced both facial and hind paw mechanical allodynia in diabetic neuropathic mice, which was closely related to the regulation of p-AMPK/p-mTOR activation in the TG and p-p38 regulation in the TNC.