Brain cholinergic and dopaminergic functions in streptozotocin induced diabetic rats: effects of curcumin and vitamin D3 supplementation

Description

Diabetes mellitus is a common metabolic disorder characterised by hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both (Feldman, 1997). Diabetes mellitus is known to be associated with neurological complications in both the peripheral nervous system (PNS) and the central nervous system (CNS) (Greene, 1999). Even though insulin secretion is mainly regulated by changes in circulating concentrations of glucose and other metabolic fuels, stimuli such as neurotransmitters and gastrointestinal hormones makes an important contribution to the overall regulation of pancreatic beta cell function. Controlling blood sugar is essential for avoiding long-term complications of diabetes like learning and memory deficit. Greater understanding of CNS involvement could lead to new strategies to prevent or reverse the damage caused by diabetes mellitus. Acetylcholine, a major neurotransmitter from the autonomic nervous system, regulates the cholinergic stimulation of insulin secretion, through interactions with muscarinic receptors (Satin & Kinard, 1998; Ahren, 2000; Gilon & Henquin, 2001). Dopamine in the CNS is involved in the control of both motor and emotional behaviour (Vallone et al., 2000) and peripherally modulates insulin secretion in the pancreatic islets (Nogueira et al., 1994)

The autonomic nervous system plays a prominent role in the regulation of insulin secretion. It has been proposed that neuronal afferent signals delivered to the pancreatic ����-cell through the vagus are responsible for the cephalic phase of insulin secretion. These effects are mediated by acetylcholine, which is released from nerve terminals and acts upon muscarinic cholinergic receptors in the ����-cell plasma membrane (Sharp et al., 1974; Berthoud et al., 1980; Mathias et al., 1985; Ahren, 2000). Cholinergic agonist carbachol increases insulin secretion from isolated rat islets (Zawalich, 1989b). Carbachol stimulated insulin secretion is inhibited by atropine.