Neuropathy, a common complication of human diabetes, is not prevented by
current antidiabetic therapy. Several mechanisms, some reversible, have
been proposed. Clinical assessment of drug efficacy in this condition is
difficult because of its slow and unpredictable development and its
possible irreversibility, once established. A reliable animal model of
diabetic neuropathy would be very useful. Changes such as reduced nerve
conduction velocity are used as models but their relationship to
neuropathy is uncertain. The main purpose of this study was to examine
autonomic changes in the experimentally diabetic rat with the aim of
identifying more appropriate models. The effects of three treatments
which correct specific biochemical abnormalities which may underlie
diabetic complications, were also studied. [Continues.]
A Doctoral Thesis. Submitted in partial fulfilment of the requirements for the award of Doctor of Philosophy at Loughborough University.
This work was supported by the British Diabetic Association and by
Imperial Chemical Industries.