Biochemical scenario behind initiation of diabetic retinopathy in type 2 diabetes mellitus

Abstract

Purpose:Despite the disease having similar glycemic status and duration microangiopathy in some patients develop within few years whereas it doesn't appear as a health complication in some diabetics for a considerable period. This study is undertaken to assess the hyperglycemia-induced biochemical background behind the development of diabetic retinopathy (DR) in type 2 diabetes mellitus (DM).Methods:Following proper diagnosis, 100 patients of type 2 DM of 10–12 years duration having no DR, and 42 patients of type 2 DM of the same duration and glycemic status as the second group, with mild retinopathy were recruited in the study. Lactic acid, glutamate, malondialdehyde (MDA), nitrate, advanced glycation end-products (AGEs), peripheral blood mononuclear cell reactive oxygen species (ROS), vascular endothelial growth factor (VEGF), and its receptor 2 (VEGFR2) in these two groups were produced in an assay following standard methodology.Results:Biochemical markers of anaerobic glycolysis, lipid peroxidation, AGEs, glutamate concentration, oxidative stress, and expression of VEGF and its VEGFR2 with significantly elevated markings were found in them who developed earliest stage of DR rather than them who had not.Conclusion:Hyperglycemia-induced anomalous glucose metabolism, lipid peroxidation, advanced glycation, glutamate toxicity, and oxidative stress create a background where apoptosis of retinal capillary endothelial cells invite increased expression of VEGF and VEGFR2, these being the crucial factors behind the development of diabetic microangiopathy.

Visual contrast sensitivity could be an early marker of diabetic retinopathy

“…Less production of adenosine triphosphate (ATP) impairs the autoregulatory systems of retinal microcirculation and the function of highly metabolically active cone receptors. Insidious apoptosis of neural and microvascular cells on one side and dysregulated microcirculation on the other side, converge to result in retinal ischemia, which is liable to impair the most sensitive visual function namely, CS ( Mondal et al., 2018 ).…”

Advanced Glycation End Products (AGEs) May Be a Striking Link Between Modern Diet and Health

“…Crosslinking of skin collagen, carotid thickening, ischemic heart attack, chronic and end-stage renal disease, diabetic retinopathy, uremic cardiomyopathy, alterations in lipo-and apolipoproteins, inactivation of nitric oxide [64,[70][71][72][73][74][75][76][77][78][79][80][81][82][83] Alzheimer's disease, certain neurodegenerative diseases, advance stages of amyloidosis β-amyloid protein plaques, cerebrovascular amyloid deposits, neurofibrillary tangles [85][86][87] Ovarian dysfunction, polycystic ovarian syndrome, anovulation, infertility Increased testosterone, thyroid hormones, androgens, anti-Mullerian hormone, disruptive steroidogenesis [71,92,108] Inflammation, allergies, asthma, multiple sclerosis, Crohn's disease Activating unprogrammed cell death, altering immune responses by monocytes, basophils, macrophages, and dendritic cells, might create false allergic responses [75,76,114,115] Dental disorders Periodontitis leading to tooth loss due to gum infection might increase the risk of heart and lung diseases [116]…”

Posibilidades de la terapia antioxidante en diabetes mellitus tipo 2. Estudio del estrés oxidativo en una muestra poblacional de pacientes diabéticos

“…Estos niveles elevados de glucosa en forma sostenida favorecen el desbalance entre la disponibilidad de óxido nítrico endotelial y la acumulación de ERO, lo cual despierta una Rodolfo Núñez-Musa, Alberto J. Núñez-Sellés, Wilfredo Mañón Rossi, Rafael Guillén Marmolejos, Gregorio Martínez-Sánchez y Antonio Selman-Almonte cadena de eventos fisiopatológicos que conducen a la disfunción enzimática en la homeostasis endotelial y a fallas en la expresión genética de los sistemas enzimáticos reguladores, a la inflamación y al EO microvascular [5][6][7][8][9]28 . Por ejemplo, en la patogénesis de la retinopatía diabética (RPD), el metabolismo de la glucosa anómala inducida por la HG, la peroxidación lipídica, la glicación avanzada, la toxicidad del glutamato y el EO crean un sustrato donde la apoptosis de células endoteliales capilares de la retina favorece una mayor expresión del factor de crecimiento endotelial vascular (VEGF, en inglés) y su receptor tipo 2 (VEGFR2, en inglés), siendo estos los factores cruciales detrás del desarrollo de la microangiopatía diabética 29 .…”