Overview

Diabetes Mellitus is a metabolic disorder associated with insulin deficiency, which not only affects the carbohydrate metabolism but also is associated with various central and peripheral complications. Chronic hyperglycemia during diabetes mellitus is a major initiator of diabetic microvascular complications like retinopathy, neuropathy, nephropathy (Sheetz & King, 2002). Glucose processing uses a variety of diverse metabolic pathways. Chronic hyperglycemia can induce multiple cellular changes leading to metabolic disorders. The central nervous system (CNS) neurotransmitters play an important role in the regulation of glucose homeostasis. These neurotransmitters mediate rapid intracellular communications not only within the central nervous system but also in the peripheral tissues. They exert their function through receptors present in both neuronal and non neuronal cell surface that trigger second messenger signaling pathways (Julius, et al., 1989). Neurotransmitters have been reported to show significant alterations during hyperglycemia resulting in altered functions causing neuronal degeneration (Kaur, et al., 1999). Neurochemical and neuro-imaging evidences have been reported to show regionally selective sympathetic denervation in diabetic neuropathy (Goldstein, et al., 2002). The changes in the brain monoamines during experimental diabetes have been reported. The serotonin content is doubled in the hypothalamus with no apparent alteration of its metabolite 5-hydroxy indole acetic acid (5-HIAA) levels, suggesting a reduced release. In the brain stem, serotonin and dopamine with the relative metabolites 5-HIAA and dihydroxyphenylacetic acid (DOPAC) are significantly reduced whereas noradrenaline is markedly increased (Chen, 1992). Insulin deficiency is the major factor involved as a trigger of the monoaminergic changes in the diabetic brain; Streptozotocin-induced diabetes produced marked alterations of monoamine concentrations in the brain regions of rats (Shimzu, 1991; Chen & Yang, 1991). The effects of streptozotocin (STZ)-induced diabetes on dopamine and serotonin release in striatum revealed that striatal dopamine release increased in acute diabetic state and this release depleted during the chronic state.

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