Diabetic polyneuropathy and insulin secretion in type II diabetic patients

Eur Neurol. 1987;27(4):251-7. doi: 10.1159/000116165.

Abstract

Electrophysiological examination was performed on 50 type II diabetic patients to verify whether insulin secretory reserve is a factor influencing the susceptibility to develop polyneuropathy. The results showed that less significant metabolic derangement related to high insulin secretory reserve, and not the high insulin secretory reserve by itself, may prevent the development of neuropathic disorders. These data are consistent with the current opinion that diabetic polyneuropathy is the consequence of the metabolic derangement caused by chronic hyperglycemia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Blood Glucose / metabolism
  • Diabetes Mellitus, Type 2 / physiopathology*
  • Diabetic Neuropathies / physiopathology*
  • Electric Stimulation
  • Female
  • Glycated Hemoglobin / metabolism
  • H-Reflex
  • Humans
  • Insulin / blood*
  • Islets of Langerhans / physiopathology
  • Male
  • Middle Aged
  • Motor Neurons / physiology
  • Neural Conduction
  • Peripheral Nerves / physiopathology
  • Sensation / physiology

Substances

  • Blood Glucose
  • Glycated Hemoglobin A
  • Insulin