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 fi-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 sorbitol compared to controls. While after 24
weeks of diabetes, the diabetic sciatic nerves showed significant
increases in glucose, fructose 1,6- bisphosphate, fructose, sorbitol
(P<0.001), lactate and ATP (P<0.05) compared to 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, 0-hydrant
butyrate, acetoacetate (P<0.001) and plasma osmolality (P<0.05)
compared to 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 contribution to the etiology of diabetic peripheral neuropathy. The present study suggests that fructose
and sorbitol accumulation with the osmotic desequilibrium and nonenzymatic
glycation of macromolecules by fructose contribute to the
mechanism of diabetic peripheral neuropathy. |
