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Insulin‐like Growth Factor‐I and IGF‐I Receptors in Diabetic Patients with Neuropathy
Author(s) -
Migdalis I.N.,
Kalantzis L.,
Samartzis M.,
Kalogeropoulou K.,
Nounopoulos C.,
Bouloukos A.
Publication year - 1995
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.1995.tb02086.x
Subject(s) - medicine , endocrinology , peripheral neuropathy , diabetes mellitus , diabetic neuropathy , receptor , insulin like growth factor , insulin , growth factor
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, HbA 1 , C‐peptide, and insulin. The neuropathy study group had significantly lower levels of IGF‐I:144.5 ng mI ‐1 (57.5–363.0, 95% confidence limits) compared to controls: 186.2 ng mI ‐1 (93.3–371.5), p <0.01, and to diabetic patients without neuropathy: 173.7 ng mI ‐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 times 10 3 (13.08–38.01) vs control subjects: 28.1 times 10 3 (18.62–42.65), p <0.01, and non‐neuropathic diabetic patients: 26.3 times 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 , 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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