Diabetes mellitus is a complex metabolic disorder which is resulting from either insulin insufficiency or insulin dysfunction. Type 1 diabetes is caused due to insulin insufficiency because of lack of functional beta cell. Type 2 diabetes are unable to respond insulin. Type II diabetes is the more common and 90% of the diabetic population in the world. Pathophysiological experimental evidences suggest the involvement of free radicals in the pathogenesis of diabetes and development of the diabetic complication. Abnormalities produced in lipids and proteins are the major etiologic factors in diabetic complication development. Free radicals are capable of damaging cellular molecules, DNA, proteins and lipids leading to altered cellular function of patients. In diabetic patients extra cellular and long-lived proteins such as elastin, lamina, and collagen are the major targets of free radicles. These proteins are modified to form glycoproteins because of hyperglycaemia. These modifications of proteins present in tissue are associated with the development of diabetic complication such as cataracts, microangiopathy, atherosclerosis and nephropathy [1,2].
Author(s) Details:
Neeli Rose Beck,
Department of Pharmacy, Guru Ghasidas Vishwavidyalaya, Bilaspur,
Chhattisgarh, India.
Dimpi Dewangan,
Department
of Pharmacy, Guru Ghasidas Vishwavidyalaya, Bilaspur, Chhattisgarh, India.
Rishika Gupta,
Department of Pharmacy, Guru Ghasidas Vishwavidyalaya, Bilaspur,
Chhattisgarh, India.
Sourabh Ghosh,
Department of Pharmacy, Guru Ghasidas Vishwavidyalaya, Bilaspur,
Chhattisgarh, India.
Ashwani Jangde,
Department of Pharmacy, Guru Ghasidas Vishwavidyalaya, Bilaspur, Chhattisgarh,
India.
Please see the link here: https://stm.bookpi.org/HATD/article/view/12514
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