File Name: advanced glycation end products and diabetes type.zip
Advanced glycation end products AGEs are formed in vivo by a non-enzymatic reaction of proteins with carbohydrates and accumulate in many tissues during ageing. They are discussed as being responsible for many age- and diabetes-related diseases. On the other hand, AGEs are formed by the heating of food and are taken up by the nutrition. The contribution of endogenously formed versus exogenous intake of AGEs to age-related diseases is still under discussion. Fortgeschrittene Glykierungsendprodukte AGEs werden in vivo durch eine nicht-enzymatische chemische Reaktion von Proteinen mit Kohlenhydraten gebildet und reichern sich in vielen Geweben mit dem Alter an.
Riset kesehatan dasar Depkes RI; Diabetes and advanced glycation end products. Diabetes Care. Increasing prevalence of the metabolic syndrome among u. Glucose, advanced glycation end products, and diabetes complications: What is new and what works. Clinical Diabetes. Vlassara H, Striker GE.
The role of advanced glycation end-products in the etiology of insulin resistance and diabetes. US Endocrinology. Insulin resistance and type 2 diabetes in high-fat-fed mice are linked to high glycotoxin intake. Oral glycotoxins determine the effects of calorie restriction on oxidant stress, age-related diseases, and lifespan. Am J Pathol. Reduced oxidant stress and extended lifespan in mice exposed to a low glycotoxin diet association with increased AGER1 expression.
Advanced glycation end products in foods and practical guide to their reduction in the diet. J Am Diet Assoc. Orally absorbed reactive glycation products glycotoxins : An environmental risk factor in diabetic nephropathy. Dietary glycotoxins: Inhibition of reactive products by aminoguanidine facilitates renal clearance and reduces tissue sequestration.
Advanced glycoxidation end products in commonly consumed foods. Protection against loss of innate defenses in adulthood by low advanced glycation end products AGE intake: Role of the antiinflammatory AGE receptor J Clin Endocrinol Metab. Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy. Am J Physiol Cell Physiol. Role of megalin in endocytosis of advanced glycation end products: Implications for a novel protein binding to both megalin and advanced glycation end products.
J Am Soc Nephrol. Restriction of dietary glycotoxins reduces excessive advanced glycation end products in renal failure patients. Open Journal Systems. Journal Help. User Username Password Remember me.
Notifications View Subscribe. Font Size. Abstract Terapi nutrisi medik telah diketahui memiliki peranan penting dalam penatalaksanaan diabetes dan komplikasinya.
Anjuran pengaturan makan saat ini menitikberatkan pada zat-zat gizi, atau pembatasan kalori, namun belum memperhatikan metode pengolahan makanan. Advanced glycation end products AGEs terbentuk akibat panas dalam proses pengolahan makanan, sebagai reaksi spontan antara gula dengan protein atau lemak; diperkirakan terbentuk akibat kondisi hiperglikemia dalam diabetes. Makanan yang lazim dikonsumsi saat ini kebanyakan melalui pemprosesan suhu tinggi heat-processed , sehingga berdampak pada meningkatnya kadar AGEs.
Full Text: PDF. Standard of medical care. Advanced glycation end products. Remember me.
Hyperglycemic conditions and disruptions to glucose-regulating pathways lead to increased formation of highly reactive aldehydes, methylglyoxal and glyoxal, which react with certain arginine and lysine residues in proteins to form advanced glycation end products AGEs. These AGEs damage the integrity of the retinal vasculature predominantly through two mechanisms: non-receptor-mediated damage, which pertains to the interaction with extracellular matrix and its functional properties, and receptor-mediated damage through AGE interactions with their receptors RAGE on pericytes and Muller cells. Both mechanisms result in increased permeability of endothelial tight junctions, and this increased permeability can lead to leaking and eventually ischemia. Once this ischemia becomes significant, neovascularization can occur, the hallmark of proliferative diabetic retinopathy. Current pharmaceutical studies have shown the potential of AGE inhibitors, such as aminoguanidine, in decreasing AGE production, thus minimizing its effects in hyperglycemic conditions. Future research will not only continue to understand the properties of AGEs and their effects on diabetes and diabetic complications like diabetic retinopathy but will also explore how they impact other diseases.
Riset kesehatan dasar Depkes RI; Diabetes and advanced glycation end products. Diabetes Care. Increasing prevalence of the metabolic syndrome among u.
Metrics details. Traditional risk factors are insufficient to explain all cases of coronary artery disease CAD in patients with diabetes mellitus DM. Advanced glycation end-products AGEs and their receptors may play important roles in the development and progression of CAD. Hyperglycemia is the hallmark feature of DM. An increase in the incidence of both micro-and macrovascular complications of diabetes has been observed with increased duration of hyperglycemia.
Mark E. Although the features of diabetic cardiomyopathy, atherosclerosis, and nephropathy have been clinically characterized, the pathogenesis and the mechanisms underlying the abnormalities in the diabetic heart and kidney are not fully understood.
The formation of advanced glycation end products AGEs is an important biochemical abnormality that accompanies diabetes mellitus and, likely, inflammation in general. Here we summarize and discuss recent studies indicating that the effects of AGEs on vessel wall homeostasis may account for the rapidly progressive atherosclerosis associated with diabetes mellitus. Driven by hyperglycemia and oxidant stress, AGEs form to a greatly accelerated degree in diabetes. Interaction of AGEs with endothelial cells as well as with other cells accumulating within the atherosclerotic plaque, such as mononuclear phagocytes and smooth muscle cells SMCs , provides a mechanism to augment vascular dysfunction. Specifically, the interaction of AGEs with vessel wall components increases vascular permeability, the expression of procoagulant activity and the generation of reactive oxygen species ROS , resulting in increased endothelial expression of endothelial leukocyte adhesion molecules. AGEs potently modulate initiating steps in atherogenesis involving blood-vessel wall interactions, triggering an inflammatory-proliferative process and, furthermore, critically contribute to propagation of inflammation and vascular perturbation in established disease.
During long standing hyperglycaemic state in diabetes mellitus, glucose forms covalent adducts with the plasma proteins through a non-enzymatic process known as glycation. Protein glycation and formation of advanced glycation end products AGEs play an important role in the pathogenesis of diabetic complications like retinopathy, nephropathy, neuropathy, cardiomyopathy along with some other diseases such as rheumatoid arthritis, osteoporosis and aging. Glycation of proteins interferes with their normal functions by disrupting molecular conformation, altering enzymatic activity, and interfering with receptor functioning. AGEs form intra- and extracellular cross linking not only with proteins, but with some other endogenous key molecules including lipids and nucleic acids to contribute in the development of diabetic complications. Recent studies suggest that AGEs interact with plasma membrane localized receptors for AGEs RAGE to alter intracellular signaling, gene expression, release of pro-inflammatory molecules and free radicals. The present review discusses the glycation of plasma proteins such as albumin, fibrinogen, globulins and collagen to form different types of AGEs.
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