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Cardiovascular Risk Factors
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
AGEs can also form non-Maillard reactions. The second formation pathway occurs from the autooxidation of glucose and the peroxidation of lipids, known an α-oxaldehydes (Figure 5.3). And the third pathway for formation of AGEs involves the polyol pathway, where glucose is converted to sorbitol by the enzyme aldose reductase and then to fructose through enzymatic action of sorbitol dehydrogenase (Figure 5.3). Fructose metabolites (as fructose 3-phosphate) then are converted into α-oxaldehydes and interact with monoacids to form AGEs. The formation of AGEs leads to several biomarkers for in vivo formation. The most widely known AGEs are carboxymethyl-lysine (CML) (found in Maillard reactions), pentosidine and pyrraline (found in Maillard reactions), and methylglyoxal (an α-oxaldehyde).
Postimplantation diabetic embryopathy
Published in Moshe Hod, Lois G. Jovanovic, Gian Carlo Di Renzo, Alberto de Leiva, Oded Langer, Textbook of Diabetes and Pregnancy, 2018
Ulf J. Eriksson, Parri Wentzel
Sorbitol (Figure 41.7) is formed from glucose with the addition of aldose reductase (AR) and further metabolized to fructose by sorbitol dehydrogenase. In the presence of increased intracellular levels of free, nonphosphorylated glucose, an increased amount of sorbitol is formed, and accumulated, due to the low capacity of sorbitol dehydrogenase. This accumulation of sorbitol is likely to be part of the pathogenesis of diabetic complications,164,165 e.g., neuropathy, nephropathy,166 and retinopathy, but it has also been suggested to have a role in diabetic embryopathy.
AGE-RAGE Axis in the Aging and Diabetic Heart
Published in Sara C. Zapico, Mechanisms Linking Aging, Diseases and Biological Age Estimation, 2017
Karen M. O’Shea, Ann Marie Schmidt, Ravichandran Ramasamy
Glucose metabolism via the polyol pathway plays an important role in the generation of reactive carbonyl intermediates and AGEs. Aldose reductase, encoded by the human gene AKR1B1, is a cytoplasmic enzyme that reduces aldehydes. As the rate-limiting enzyme that catalyzes the first step of the polyol pathway, aldose reductase converts glucose to sorbitol in a NADPH-dependent manner. Sorbitol is then converted to fructose by sorbitol dehydrogenase at the cost of depletion of NAD+. Sorbitol and fructose accumulate in diabetic hearts when flux through the polyol pathway is increased due to high levels of glucose, leading to the generation of AGEs (Chung and Chung 2003). Fructose can be phosphorylated by fructose-3-phosphokinase into fructose-3-phosphate, which itself can modify and directly interact with proteins, lipids, and nucleic acids or be converted into AGE precursor3-deoxyglucosone. Additionally, the depletion of NAD+ and increased NADH/NAD+ that occurs as a result of increased flux through the polyol pathway inhibits NAD+-dependent enzymes, including GAPDH. This results in accumulation of glyceraldehyde-3-phosphate and dihydroxyacetone phosphate, both of which are precursors for methylglyoxal (Rabbani and Thornalley 2015).
Biomarkers in diabetic neuropathy
Published in Archives of Physiology and Biochemistry, 2023
Kaveri M. Adki, Yogesh A. Kulkarni
Hyperglycaemia activates the polyol pathway. Aldose reductase utilises excess glucose and converts into sorbitol. Similarly, sorbitol dehydrogenase converts sorbitol into fructose. This cellular mechanism depletes nicotinamide adenine dinucleotide phosphate (NADPH), which causes the generation of glutathione. Glutathione is the primary antioxidant in nerve tissue. The depletion of glutathione leads to oxidative stress and slows down nerve conduction. A study by Varkonyi et al. showed that AGEs play a prime role in the progression of various diabetic complications such as duplication of basal lamina around endothelial cells results in thickening of walls of small blood vessels (Várkonyi et al. 2017). The AGEs result in excess glucose and protein complex formation. These AGEs form a complex network with collagen and harm nerves (Grisold et al. 2017).
Diabetic eye: associated diseases, drugs in clinic, and role of self-assembled carriers in topical treatment
Published in Expert Opinion on Drug Delivery, 2021
Axel Kattar, Angel Concheiro, Carmen Alvarez-Lorenzo
Hyperglycemia is also responsible for triggering the polyol pathway. Under normoglycemic conditions, the Embden–Meyerhof–Parnas catabolism route that transforms glucose into pyruvate, NADH, and ATP becomes saturated. Consequently, the polyol pathway, which commonly transforms 3% glucose, enters into action with the participation of two enzymes: (i) aldose reductase that transforms glucose into sorbitol with the consumption of NADPH and (ii) sorbitol dehydrogenase that slowly converts sorbitol into fructose while consuming NAD+. The polyol pathway, which is very active in retina and lens, metabolizes more than 30% glucose under diabetic conditions [73]. Accumulation of sorbitol causes osmotic stress, triggers leukocyte accumulation, disrupts blood-retinal barrier, favors cells apoptosis, and starts a cascade of oxidative stress-mediated reactions [74]. The excess of fructose acts as precursor of advanced glycation-end products (AGEs). In this context, aldose reductase inhibitors are gaining increased attention, and epalrestat is approved in some countries for oral administration. As an alternative, drugs that accelerate the metabolic rate of sorbitol dehydrogenase and, thus, decrease the levels of sorbitol are being tested [73].
The Beneficial Radioprotective Effect of Tomato Seed Oil Against Gamma Radiation–Induced Damage in Male Rats
Published in Journal of Dietary Supplements, 2018
Magda K. Ezz, Nashwa K. Ibrahim, Mahmoud M. Said, Mostafa A. Farrag
Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were determined by the method of Reitman and Frankel (1957); serum urea and creatinine concentrations were determined by the methods of Fawcett and Scott (1960) and Bartels et al. (1972), respectively, using commercial assay kits (Biodiagnostic, Egypt). Serum total cholesterol, triacylglycerol (TAG), and high-density lipoprotein cholesterol (HDL-C) concentrations were determined according to the method of Young (1990) using commercial assay kits (N.S BIOTEC, Egypt). Low-density lipoprotein cholesterol (LDL-C) and very-low-density lipoprotein cholesterol (VLDL-C) levels were calculated according to Friedewald et al. (1972); the atherogenic index of plasma (AIP) was calculated according to Holmes et al. (2008) [AIP = log10 (TAG/HDL-C)], in which TAG and HDL-C concentrations were expressed as mmol/L. Lipid peroxidation (LPO) was determined in tissue homogenates in terms of thiobarbituric acid reactive substances expressed as malondialdehyde (MDA) according to the method of Yoshioka et al. (1979); superoxide dismutase (SOD) activity was determined in tissue homogenates according to the method of Minami and Yoshikawa (1979). Serum total testosterone level was determined by a competitive enzyme-linked immunosorbent assay using a commercial kit provided by Monobind Inc. (CA, USA). Serum sorbitol dehydrogenase (SDH) level was determined by a sandwich enzyme–linked immunosorbent method using an assay kit provided by Wkea Med Supplies Corp. (China); serum level of vascular cell adhesion molecule-1 (VCAM-1) was determined by a sandwich enzyme–linked immunosorbent method using an assay rat kit provided by MyBiosource (USA).