Metabolic alterations associated with T2D are well characterised by epidemiological and research primarily based scientific studies. The pathogenesis and development of T2D is ascribed to 4 mechanisms; elevated State-of-the-art glycation stop products (AGE) formation, elevated polyol pathway flux, activation of protein kinase C (PKC) isoforms, and greater hexosamine pathway flux[7]. https://www.directivepublications.org/journal-of-diabetology-research/