Biochemical Studies of CNS and PNS in Human and Experimental Diabetes

Abstract

Neuropathological evidence of encephalopathy and neuropathy has been found in all autopsied patients with long-term juvenile diabetes. Earlier biochemical studies of human post mortem specimens indicated extensive biochemical damage of the diabetic peripheral nerve but not of the brain. The activities of acid proteinase and phosphatase, β-glucosidase, β-glucosaminidase, glucose-6-phosphatase, succinyl dehydrogenase (SDH), and 2’,3’-cyclic nucleotide-3’-phosphohydrolase (CNP) were now measured from the brain homogenates of rats made diabetic with streptozotocin at the age of 1 month and killed after 1, 3, 6 and 15 months. The activities of acid proteinase and β-glucosidase decreased and that of SDH increased at the beginning of the experiment. A slight increase of acid phosphatase was noted at the end and a slight decrease of β-glucosaminidase at the beginning. The activities of SDH and CNP increased throughout the experiment both in the diabetic and control animals, probably due to maturation. In general, experimental streptozotocin diabetes induced few, transient and not very significant changes in enzymes known to be connected with myelination and demyelination in the CNS. The findings agree with those obtained previously for human diabetic specimens.