DIABETIC NEUROPATHY AND ENCEPHALOPATHY

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.

Autorentext

El Dr. Kanwaljit Chopra trabaja como profesor adjunto de farmacología en el Instituto Universitario de Ciencias Farmacéuticas de la Universidad de Panjab, Chandigarh (India). Sus intereses de investigación se centran en la Farmacología Inversa con énfasis en la diabetes. Tiene más de 160 publicaciones de investigación en revistas internacionales con revisión por pares.

Klappentext

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.