Objective. To explore the role of insulin-like growth factor 1 （IGF-1） gene expression abnormality in neurotrophic causes of diabetic peripheral neurophathy.Methods. Diabetes was induced in Sprague Dawley rats by alloxan. The parameters were measured as follows: IGF-1 mRNA by reverse transcriptase-polymerase chain reaction （RT-PCR）; IGF-1 peptide by enzyme-linked immunosorbent assay （ELISA）; electrophysiological parameters of nerves by evoked electromyo-gram; morphometric evaluation of sciatic nerves under light microscope and transmission electron microscope.Results. During early diabetic stage

IGF-1 mRNA [ （0. 430 ±0. 031） vs. （0. 370 ±0. 016）

P <0. 01

（0. 430 ±0. 031） vs. （0. 280 ±0. 010）

P <0. 001

respectively]

IGF - 1 peptide contents [ （38. 44 ±3. 60） ng/mgvs. （30. 06 ± 2. 41） ng/mg

P <0. 01

（38. 44 ± 3. 6） ng/mg vs. （3. 71 ±2. 70） ng/mg

P <0. 001

respectively] in sciatic nerve tissue reduced in diabetic rats with hyperglycemia and varied with severity of diabetic state when compared with non-diabetic control rats

and further gradually down-regulated in the diabetic rats with duration of diabetes [IGF-1 mRNA （0. 320 ±0. 021） - （0. 230 ±0. 060）; IGF-1 peptide （28. 80 ±3. 30） -（19. 51 ± 1. 80）ng/mg]. Furthermore

they correlated with nerve functional （sensory nerve conduction velocity: r = 0.741

P <0. 001; amplitudeofevokedpotential: r = 0.716

P <0. 001

respectively ）andstructuralabnormali-ty（axonal areas r = 0. 81

P < 0. 001） of sciatic nerve. No difference was found in the above parameters between diabetic rats with euglycemia and non-diabetic control group.Conclusion

IGF-1 gene expression in tissues was down-regulated from early diabetic stage

and varied with the severity and duration of diabetic state. The decrement in IGF-1 level might contribute to the initiation and development of diabetic neuropathy via autocrine or paracrine pathway.