Diabetes is a long-term metabolic disorder characterized by persistently elevated blood sugar levels. Chronic hyperglycemia enhances glucose–protein interactions, leading to the formation of advanced glycation end products (AGEs), which form irreversible cross-links with a wide variety of macromolecules, and accumulate rapidly in the body tissues. Thus, the objective of this study was to assess the therapeutic properties of C-phycocyanin (C-PC) obtained from Plectonema species against oxidative stress, glycation, and type 2 diabetes mellitus (T2DM) in a streptozotocin (STZ)-induced diabetic Wistar rat. Forty-five days of C-PC administration decreased levels of triglycerides (TGs), blood glucose, glycosylated hemoglobin, (HbA1c), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), liver and kidney function indices, and raised body weight in diabetic rats. C-PC suppressed biochemical glycation markers, as well as serum carboxymethyllysine (CML) and fluorescent AGEs. Additionally, C-PC maintained the redox state by lowering lipid peroxidation and protein-bound carbonyl content (CC), enhancing the activity of high-density lipoprotein cholesterol (HDL-C) and renal antioxidant enzymes, and preserving retinal and renal histopathological characteristics. Thus, we infer that C-PC possesses antidiabetic and antiglycation effects in diabetic rats. C-PC may also act as an antidiabetic and antiglycation agent in vivo that may reduce the risk of secondary diabetic complications.

In 2007, diabetes affected around 244 million people across the globe. The number of diabetics worldwide is projected to reach 370 million by 2030. With diabetes incidence reaching epidemic proportions globally, diabetic nephropathy (DN) has emerged as one of the most difficult health conditions. Although therapeutic approaches such as rigorous blood glucose and blood pressure management are successful in preventing DN, they are far from ideal, and the number of diabetic patients with end-stage renal disease continues to grow. As a result, a unique treatment approach for DN should be devised. There is mounting evidence that advanced glycation end products (AGEs), senescent macro protein derivatives generated at an accelerated pace in DN, contribute to DN by generating oxidative stress. The purpose of this article is to discuss the pathophysiological significance of AGEs and their receptor in DN.