Insulin treatment enhances expression of IGF-I in sural nerves of diabetic patients

Muscle Nerve. 2001 May;24(5):622-9. doi: 10.1002/mus.1047.

Abstract

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.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Diabetes Mellitus / drug therapy*
  • Diabetes Mellitus / metabolism*
  • Diabetes Mellitus / pathology
  • Female
  • Humans
  • Immunohistochemistry
  • Insulin / therapeutic use*
  • Insulin-Like Growth Factor I / biosynthesis*
  • Male
  • Middle Aged
  • Paraffin Embedding
  • Receptor, IGF Type 1 / biosynthesis
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sural Nerve / drug effects
  • Sural Nerve / metabolism*
  • Sural Nerve / pathology

Substances

  • Insulin
  • Insulin-Like Growth Factor I
  • Receptor, IGF Type 1