Muscarinic M1, M3, Nicotinic,GABAA and GABAB Receptor ...

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Discussion
receptors in glucose deprived condition contributes to neuronal dysfunction. An
alteration in insulin signalling ability will have a major impact on cellular energy
balance by affecting rate of uptake of glucose and other metabolic substrates and
also directly by affecting the activity of enzymes involved in carbohydrate, lipid
and protein metabolism (Dimitriadis, 2000). Many or all of the enzymes involved
in the mitochondrial tricarboxylic acid cycle, the final common catabolic
sequence, appear to be modulated by insulin independently of insulin-stimulated
glucose transport. Expression of the genes for many enzymes involved in
metabolism also appears to be regulated by insulin (O'Brien & Granner, 1996).
Thus, an alteration of insulin signalling in brain regions have a profound effect on
cellular energetic and is a contributing factor in the energetic deficit associated
with the development of diabetes associated neurodegenerative diseases.
Generalized impairment in the activation of the sympathoadrenal system in
response to stress is mediated by CNS insulin receptors (Fischer et al, 2005).
While the brain has classically been regarded as insulin insensitive, there has been
clinical evidence to implicate that insulin act in the central nervous system (CNS)
to influence sympathetic nervous activity (Paramore et al., 1998). Therefore,
insulin receptor activation and subsequent stimulation of insulin receptor second
messenger cascades, including the translocation of insulinsensitive GLUTs,
participate in the cognitive enhancing properties of insulin (Park, 2001; Watson &
Craft, 2003).
Pancreas
Diabetes mellitus is characterized by uncontrolled hyperglycemia and
maintenance of blood glucose within the physiological range is critical for the
prevention of diabetes-related complications. However, tight glycemic control is
also associated with an increased incidence of therapy-induced hypoglycemic
events (DCCT, 1997). Glucagon, secreted from the pancreatic α-cells, counters the
actions of insulin and corrects hypoglycemia by enhancing hepatic glucose output