Aim: To study the mechanism of LCs effects on peripheral neuropathy in type 2 diabetic mice.Methods: Male 3-week age mice were allocated to four groups: control, diabetes, pre-treatment and treatment (LC, 125 mg/kg BW, i.g) groups.Mice were given long term high-energy diet and twice low-dose STZ (100mg/kg, i.p) to induce type 2 diabetes.Blood glucose, tail-flick latency, LC, insulin and IGF-1 in plasma were measured in this study.Morphology of sciatic nerve fibers was observed under electron microscope.Results:Plasma LC was decreased by 38.9% in type 2 diabetic mice (P<0.01), accompanied with hyperalgesia in tail-flick test (P<0.01).Administration of LC increased plasma insulin levels by 91.6% (P<0.01) and alleviated diabetic peripheral neuropathy, which manifested normalized tail-flick latency (P<0.01).LC reversed demyelination, axonal atrophy and mitochondria swelling in diabetic nerve fibers under electron microscope.Conclusion: LC improved peripheral neuropathy via increasing endogenous insulin level in type 2 diabetic mice.