INSULIN-LIKE GROWTH-FACTOR-I AND IGF-I RECEPTORS IN DIABETIC-PATIENTSWITH NEUROPATHY

Since a number of animal studies have shown that Insulin-like growth I (IGF-I) stimulates nerve regeneration, the aim of our study was to ev aluate the possible relationship between IGF-I and IGF-I receptors in diabetic patients with peripheral neuropathy. One hundred and four pat ients with Type 2 diabetes (57 with peripheral neuropathy and 47 nonne uropathic) were studied. Controls were 17 non-diabetic persons. After an overnight fast, blood was taken for IGF-I, IGF-I receptors, glucose , HbA(1), C-peptide, and insulin. The neuropathy study group had signi ficantly lower levels of IGF-I:144.5 ng ml(-1) (57.5-363.0, 95% confid ence limits) compared to controls: 186.2 ng ml(-1) (93.3-371.5), p<0.0 1, and to diabetic patients without neuropathy: 173.7 ng ml(-1) (83.1- 363.0), p<0.01. The study group also had a lower number of IGF-I recep tors per red cell: 22.9 x 10(3) (13.08-38.01) vs control subjects: 28. 1 x 10(3) (18.62-42.65), p<0.01 and non-neuropathic diabetic patients: 26.3 x 10(3) (16.59-41.68), p<0.01. In diabetic subjects there was a positive correlation (r = 0.20, p<0.05) between IGF-I and HbA(1), whil e in the neuropathy group there was a negative correlation between the score for nerve dysfunction with the IGF-I (r = -0.39, p<0.01) and wi th IGF-l receptors (r = -0.34, p<0.01). We conclude that in diabetic p atients with peripheral neuropathy there are abnormalities of ICF-I an d IGF-I receptors which may contribute to impaired neuronal regenerati on.