Diabetes mellitus produces numerous neurophysiological &
structural changes in the central and peripheral nervous system and
it further leads to development of neuropathic pain & moderate
cognitive deficits in diabetics. The etiology of diabetes
associated neuropathic pain & cognitive decline is
multifactorial and involves an underlying phenomenon of metabolic
memory. The concept of "metabolic memory," that is of diabetic
vascular stresses persisting even after stringent glucose control,
has been supported both in the laboratory and in the clinic in both
type 1 & type 2 diabetes. Therefore, "switching off" the
metabolic memory, could be an important strategy for the prevention
of diabetic neurological complications. Insulin alone reverses the
hyperglycemia but partially reversed neuropathic pain and memory
deficits in diabetic rats. However, insulin in combination with
tocotrienol, lycopene and sesamol not only attenuates the diabetic
condition but also reverses neuropathic pain and memory loss by
switching off various components of metabolic memory phenomenon.
Thus, these interventions may find clinical application in
therapeutic armamentarium of diabetics.
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