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Insulin treatment enhances expression of IGF‐I in sural nerves of diabetic patients
Author(s) -
Grandis Marina,
Nobbio Lucilla,
Abbruzzese Michele,
Banchi Loris,
Minuto Franceso,
Barreca Antonina,
Garrone Simona,
Mancardi Gian Luigi,
Sche Angelo
Publication year - 2001
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.1047
Subject(s) - medicine , sural nerve , endocrinology , insulin , diabetes mellitus , pathogenesis , diabetic neuropathy , peripheral neuropathy , insulin like growth factor , schwann cell , insulin receptor , receptor , growth factor , insulin resistance , pathology
We studied the expression of insulin‐like growth factor I (IGF‐I) and its receptor in sural nerves from 8 diabetic patients divided into insulin‐treated (IT) and non–insulin‐treated (NIT) groups, compared with 5 patients with axonal neuropathies and 4 control patients (undergoing biopsies for diagnostic purposes). Insulin‐like growth factor I mRNA levels did not differ in diabetic cases compared with control subjects. In sural nerves from IT patients and axonal neuropathies, IGF‐I expression was higher than in NIT subjects and diagnostic controls. Changes in IGF‐I receptor mRNA levels paralleled those of the ligand. Insulin‐like growth factor I immunoreactivity was higher in nerves undergoing axonal degeneration and higher in IT than NIT diabetic patients and diagnostic controls. These findings suggest that insulin treatment increases IGF‐I expression in diabetic nerves. Our data do not support the hypothesis of an absolute IGF‐I deficiency in human diabetic neuropathy. A Schwann cell's incapacity to increase IGF‐I expression after severe nerve damage, as happens in axonal neuropathies, may be a cofactor in the pathogenesis of diabetic neuropathy. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 622–629, 2001.