Peripheral neuropathy is the most common and perhaps the most devastating
complication associated with diabetes mellitus. Many theories regarding the
pathogenesis of diabetic peripheral neuropathy has been proposed. The present study
was designed to investigate the problem of the pathogenesis of diabetic peripheral
neuropathy. Thirty male albino rats were made diabetic by streptozotocin intravenous
injection (65 mg/kg) and another thirty rats were used as a control group. Sciatic
nerves were surgically removed from both diabetic and control rats and were used for
the estimation of glucose, pyruvate, lactate, ATP, fructose, sorbitol and myoinositol.
Plasma levels of sodium, potassium, glucose, lactate, acetoacetate, P-hydroxy butyrate
and osmolality were also measured. In the diabetic sciatic nerves, after 4 weeks of the
induction of diabetes, there were significant increases (P<0.001) in glucose, fructose
and sorbito! cerspared to the coati-01s. While after 24 weeks of diabetes, the diabetic
sciatic nerves showed significant increases in glucose, fructose, sorbitol (P<0.001),
lactate and ATP (P<0.05) compared to the controls. In the diabetic rats, after 4 and 24
weeks of the induction of diabetes, there were significant increases in the plasma
levels of glucose, p-hydroxy butyrate, acetoacetate (13<0.001) and plasma osmolality
(P<0.05) compared to the control rats. While after 24 weeks of diabetes, the diabetic
rats showed significant increases in the plasma levels of potassium (P<0.05) and
lactate (P<0.001) compared to the control rats. So, we could conclude that the
metabolic abnormalities combine to produce deleterious changes that make a major
oc,rtil-n+i?-1 to thc ot'slogy ofdiztotiz .i.:..isopathy. The psscut study
suggests that fructose and sorbitol accumulation with the osmotic disequilibrium and
non-enzymatic glycation of macromolecules by fructose contribute to the mechanism
of diabetic peripheral neuropathy. |
