Inhibition of advance glycation end products formation, gastrointestinal digestion, absorption and toxicity: A comprehensive review

Prunin from Poncirus trifoliata (L.) Rafin Inhibits Aldose Reductase and Glucose-Fructose–Mediated Protein Glycation and Oxidation of Human Serum Albumin

“…The process of glycation, which is the irreversible nonenzymatic interaction between reducing sugars and proteins, lipids, or nucleic acids, results in the heterogeneous substances known as AGEs . Protein glycation typically occurs in both hyperglycemic and normal conditions, but the etiology of diabetes complications is due largely to exposure to hyperglycemic conditions, which trigger multiple metabolic pathways, including the polyol pathway, the protein kinase C (PKC) pathway, and the generation of AGEs . AGEs, which can be endogenous or exogenous, have been related to the progress of diabetes complications such as vascular problems, retinopathy, atherosclerosis, and renal failure. , Excessive AGE formation in tissues promotes the progress and development of diabetic complications, and blocking glycated progression is regarded as an important way of resolving AGE-initiated diabetes complications.…”

“…A nonfluorescent AGE, CML serves as a marker for the generation of AGEs caused by oxidatively breaking down an Amodori product, or by a polyol route driven by α-oxoaldehydes such as methylglyoxal, glyoxal, and 3-deoxyglucosone. , The formation of CML, one of the most chemically described AGEs in humans, , occurs through oxidative degradation driven by hydroxyl radicals of Amadori products and during the metal-catalyzed oxidation of polyunsaturated fatty acids in protein-containing conditions . Furthermore, CML is a prevalent AGE in vivo, is typically not fluorescent, and is detected most often in the kidneys of individuals with diabetes . CML and other AGEs have also been detected in the blood vessels of the retina in individuals with type 2 diabetes (T2D).…”

“…The effects of varying substrate concentrations were monitored in order to identify the impact of enzyme inhibition caused by the three test flavonoids at various concentrations. The inhibition type was assessed using various concentrations of DL -glyceraldehyde (40,20, and 10 mM) as a substrate in the presence of varying concentrations of the test flavonoids in Lineweaver−Burk double reciprocal plots (1/enzyme velocity [1/V] versus 1/substrate concentration [1/[S]]). The RLAR kinetic analysis was conducted using the following test flavonoid concentrations: 0.5, 2.5, and 10 μM for prunin; 0.5, 2, and 10 μM for naringin; and 0.5, 2.5, and 10 μM for narirutin.…”

“…6,40 The formation of CML, one of the most chemically described AGEs in humans, 9,40 occurs through oxidative degradation driven by hydroxyl radicals 40 of Amadori products and during the metalcatalyzed oxidation of polyunsaturated fatty acids in proteincontaining conditions. 11 Furthermore, CML is a prevalent AGE in vivo, is typically not fluorescent, 40 and is detected most often in the kidneys of individuals with diabetes. 42 CML and neuropathy and microangiopathy.…”

“…40 AGEs, which can be endogenous or exogenous, have been related to the progress of diabetes complications such as vascular problems, retinopathy, atherosclerosis, and renal failure. 5,40 Excessive AGE formation in tissues promotes the progress and development of diabetic complications, and blocking glycated progression is regarded as an important way of resolving AGEinitiated diabetes complications. AGE is typically produced by the most prevalent reducing sugars in the blood, fructose and glucose, reacting spontaneously with protein amino groups.…”