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 evaluate the possible relationship between IGF-I and IGF-I receptors in diabetic patients with peripheral neuropathy. One hundred and four patients with Type 2 diabetes (57 with peripheral neuropathy and 47 non-neuropathic) were studied. Controls were 17 non-diabetic persons. After an overnight fast, blood was taken for IGF-I, IGF-I receptors, glucose, HbA1, C-peptide, and insulin. The neuropathy study group had significantly lower levels of IGF-I:144.5 ng ml-1 (57.5-363.0, 95% confidence limits) compared to controls: 186.2 ng ml-1 (93.3-371.5), p < 0.01, 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 receptors 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 HbA1, while 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 with IGF-I receptors (r = -0.34, p < 0.01). We conclude that in diabetic patients with peripheral neuropathy there are abnormalities of IGF-I and IGF-I receptors which may contribute to impaired neuronal regeneration.
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