KAŇKOVÁ, Kateřina. Diabetic threesome (hyperglycemia, renal function and nutrition) and advanced glycation end products: evidence for the multiple-hit agent? Proceedings of the Nutrition Society. Cambridge, United Kingdom: Cambridge University Press, 2008, roč. 67, č. 1, s. 60-74. ISSN 0029-6651.
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Základní údaje
Originální název Diabetic threesome (hyperglycemia, renal function and nutrition) and advanced glycation end products: evidence for the multiple-hit agent?
Název česky Diabetic threesome (hyperglycemia, renal function and nutrition) and advanced glycation end products: evidence for the multiple-hit agent?
Autoři KAŇKOVÁ, Kateřina (203 Česká republika, garant).
Vydání Proceedings of the Nutrition Society, Cambridge, United Kingdom, Cambridge University Press, 2008, 0029-6651.
Další údaje
Originální jazyk angličtina
Typ výsledku Článek v odborném periodiku
Obor 30202 Endocrinology and metabolism
Stát vydavatele Velká Británie a Severní Irsko
Utajení není předmětem státního či obchodního tajemství
Impakt faktor Impact factor: 3.981
Kód RIV RIV/00216224:14110/08:00024130
Organizační jednotka Lékařská fakulta
UT WoS 000253375200008
Klíčová slova anglicky AGEs; diabetes mellitus; diabetic nephropathy; fructosamine 3 kinase; glycation; glyoxalase; nutrigenetics; RAGE
Štítky AGEs, diabetes mellitus, diabetic nephropathy, fructosamine 3 kinase, glycation, glyoxalase, nutrigenetics, RAGE
Příznaky Mezinárodní význam, Recenzováno
Změnil Změnila: prof. MUDr. Kateřina Kaňková, Ph.D., učo 2524. Změněno: 22. 6. 2009 09:44.
Anotace
Complex chemical processes called non-enzymatic glycation operating in vivo and analogical chemical interactions between sugars and proteins occurring during thermal processing of food (know se Maillard reaction) are one of the interesting examples of potentially harmful interaction between nutrition and disease. Non-enzymatic glycation comprise a series of reactions between sugars, alpha-oxoaldehydes and other sugar derivatives and amino groups of amino acids, peptides and proteins leading to the formation of heterogeneous moieties collectively called Advanced Glycation End-products (AGEs). AGEs possess a wide range of chemical and biological properties and play a role in diabetes-related pathology as wells as in several other diseases. Diabetes is, nevertheless, of main interest for several reasons: (i) chronic hyperglycemia feeds the substrates for the extra- as well as intracellular glycation, (ii) hyperglycaemia-induced oxidative stress accelerates AGE formation in the process of glycoxidation, (iii) AGE-modified proteins are subjects of rapid intracellular proteolytic degradation releasing free AGE-adducts into the circulation where they can bind to several pro-inflammatory receptors, especially Receptor of AGEs (RAGE), and, finally, (iv) kidneys, which are principally involved in the excretion of free AGE-adducts, might be damaged by diabetic nephropathy and this further enhances AGE-toxicity because of diminished AGE clearance. Increased dietary intake of AGEs in highly processed foods might represent an additional, exogenous, metabolic burden on top of those already present endogenously in diabetics. Finally, interindividual genetic and functional variability in genes encoding enzymes and receptors involved in either formation or degradation of AGEs could have a significant pathogenic, nutrigenomic and nutrigenetic consequences.
Anotace česky
Complex chemical processes called non-enzymatic glycation operating in vivo and analogical chemical interactions between sugars and proteins occurring during thermal processing of food (know se Maillard reaction) are one of the interesting examples of potentially harmful interaction between nutrition and disease. Non-enzymatic glycation comprise a series of reactions between sugars, alpha-oxoaldehydes and other sugar derivatives and amino groups of amino acids, peptides and proteins leading to the formation of heterogeneous moieties collectively called Advanced Glycation End-products (AGEs). AGEs possess a wide range of chemical and biological properties and play a role in diabetes-related pathology as wells as in several other diseases. Diabetes is, nevertheless, of main interest for several reasons: (i) chronic hyperglycemia feeds the substrates for the extra- as well as intracellular glycation, (ii) hyperglycaemia-induced oxidative stress accelerates AGE formation in the process of glycoxidation, (iii) AGE-modified proteins are subjects of rapid intracellular proteolytic degradation releasing free AGE-adducts into the circulation where they can bind to several pro-inflammatory receptors, especially Receptor of AGEs (RAGE), and, finally, (iv) kidneys, which are principally involved in the excretion of free AGE-adducts, might be damaged by diabetic nephropathy and this further enhances AGE-toxicity because of diminished AGE clearance. Increased dietary intake of AGEs in highly processed foods might represent an additional, exogenous, metabolic burden on top of those already present endogenously in diabetics. Finally, interindividual genetic and functional variability in genes encoding enzymes and receptors involved in either formation or degradation of AGEs could have a significant pathogenic, nutrigenomic and nutrigenetic consequences.
Návaznosti
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