Diabetes mellitus is known to impair
glucose metabolism. The fundamental mechanism underlying hyperglycaemia in
diabetes mellitus involves decreased utilization of
glucose by the brain. However, mechanisms responsible for progressive failure of glycaemic regulation in type I (
IDDM) diabetes need extensive and proper understanding. Hence the present study was initiated. Type I diabetes was induced in albino rat models with
alloxan monohydrate (40 mg/Kg iv). Cerebral cortex and medulla oblongata were studied 48 h after alloxanisation. Diabetes caused an elevation in
glucose,
glutamate,
aspartate,
GABA and
taurine levels and a decline in the
glutamine synthetase activity. The activities of brain
lactate dehydrogenase (LDH) and
pyruvate dehydrogenase (PDH) exhibited significant decrease during diabetes.
Ammonia content increased (P < 0.01) as a function of diabetes. Na(+)-K(+)
ATPase showed an elevation (P < 0.01) and Ca(++)-
ATPase activity decreased (P < 0.01).
Calcium content enhanced (P < 0.05) in the brain of diabetic rats. A General increase in the brain
AMP,
ADP and
ATP was found on inducing diabetes. Impaired cerebral
glucose metabolism accounts for the failure of cerebral
glucose homeostasis. The impairment in the glycaemic control leads to disturbances in cerebral
glutamate content (resulting in
calcium overload and excitotoxic injury) and brain energy metabolism as reflected by alterations occurring in
adenine nucleotide and the
ATPases. The failure in the maintenance of normal energy metabolism during diabetes might affect
glucose homeostasis leading to gross cerebral dysfunction during diabetes.