Glycosylation End Products Advanced
Mostrando 1-12 de 23 artigos, teses e dissertações.
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1. O efeito pró-apoptótico de oligômeros da amilina humana não é potencializado pela lipotoxicidade em ilhotas pancreáticas de rato em cultura / The pro-apoptotic effect of human amylin oligomers is not potentiated by lipotoxicity in rat pancreatic islets in culture
The amyloid deposit is a common histopathological feature in patients with type 2 diabetes mellitus (T2DM) and it seems to be related to the pancreatic beta cell dysfunction characteristic of this disease. A study previously developed in our laboratory found that human amylin oligomers decrease mRNA expression of the glucose-dependent insulinotropic polypept
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 25/07/2012
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2. Benfotiamina e Mito Q protegem ilhotas pancreáticas de rato em cultura dos efeitos pró-apoptóticos dos produtos finais de glicação avançada (AGEs) / Benfotiamine and Mito Q protect rat pancreatic islets in culture from pro-apoptotic effects of advanced glycation end products
A perda da função das células beta acelera a deterioração do controle metabólico em pessoas com diabetes tipo 2. Além da lipo- e da glicotoxicidade, os AGEs parecem contribuir para esse processo, promovendo a apoptose das ilhotas pancreáticas. Em outros tecidos, os AGEs interagem com seu receptor específico (RAGE), produzindo espécies reativas de o
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 13/03/2012
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3. Albumina modificada por glicação avançada no diabete melito tipo 1 e 2 prejudica o transporte reverso de colesterol e favorece o acúmulo de lípides em macrófagos / Impairment in reverse cholesterol transport and macrophage lipid accumulation induced by advanced glycated albumin drawn from uncontrolled type 1 and type 2 diabetes mellitus patients
Advanced glycation end products are prevalent in diabetes mellitus and alter lipids and lipoprotein metabolism. In this study we analyzed the role of albumin, isolated from control individuals (C, n = 12) and uncontrolled type 1 (DM 1, n = 13) and type 2 (DM 2, n = 11) diabetes mellitus patients on macrophage cholesterol removal, intracellular lipid accumula
Publicado em: 2011
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4. Supramolecular organization, spatial orientation and optical properties of extracellular proteins in corneas and aortas from diabetic spontaneous mice / Organização supramolecular, orientação espacial e propriedades opticas de proteinas extracelulares em conrneas e aortas de camundongos espontaneamente diabeticos
Diabetes mellitus is a chronic disorder of the carbohydrate, lipids and protein metabolism. A characteristic feature of this disorder is the hyperglycemia due to a deficient insulin production or to metabolic defects on its response in peripheral tissues. Hyperglycemia induces non-enzymatic glycosylation of proteins, which is responsible for advanced glycosy
Publicado em: 2007
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5. Advanced glycation end-products and Nuclear Factor K-B in lacrimal glands and ocular surface of diabetes and aging animal models / Avaliação dos produtos finais de glicosilação e o fator nuclear K-B em glandulas lacrimais e superficie ocular de modelos animais de diabetes e envelhecimento
Este estudo avaliou as possíveis vias comuns na fisiopatogênese da síndrome do olho seco no Diabetes Mellitus (DM) e no envelhecimento, envolvendo o acúmulo dos produtos de glicosilação ("Advanced Glycation End-products" - AGEs), seu receptor RAGE e a ativação do Fator Nuclear-?B (NF-?B) na glândula lacrimal (GL) e alterações do filme lacrimal nes
Publicado em: 2006
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6. Advanced glycosylation products quench nitric oxide and mediate defective endothelium-dependent vasodilatation in experimental diabetes.
Nitric oxide (an endothelium-derived relaxing factor) induces smooth muscle relaxation and is an important mediator in the regulation of vascular tone. Advanced glycosylation end products, the glucose-derived moieties that form nonenzymatically and accumulate on long-lived tissue proteins, have been implicated in many of the complications of diabetes and nor
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7. Lipid advanced glycosylation: pathway for lipid oxidation in vivo.
To address potential mechanisms for oxidative modification of lipids in vivo, we investigated the possibility that phospholipids react directly with glucose to form advanced glycosylation end products (AGEs) that then initiate lipid oxidation. Phospholipid-linked AGEs formed readily in vitro, mimicking the absorbance, fluorescence, and immunochemical propert
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8. Aminoguanidine inhibits oxidative modification of low density lipoprotein protein and the subsequent increase in uptake by macrophage scavenger receptors.
Aminoguanidine decreases the formation of advanced glycosylation end products that occurs during chronic hyperglycemia. Presumably this occurs because early glycosylation products preferentially bind to aminoguanidine rather than to lysine groups of adjacent proteins. Because oxidative modification of low density lipoprotein (LDL) also involves derivatizatio
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9. Exogenous advanced glycosylation end products induce complex vascular dysfunction in normal animals: a model for diabetic and aging complications.
Advanced glycosylation end products (AGEs) have been implicated in many of the complications of diabetes and normal aging. Markedly elevated vascular tissue and circulating AGEs were linked recently to the accelerated vasculopathy of end-stage diabetic renal disease. To determine the pathogenic role of AGEs in vivo, AGE-modified albumin was administered to h
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10. Increased collagen-linked pentosidine levels and advanced glycosylation end products in early diabetic nephropathy.
RATIONALE: Advanced glycosylation end products (AGEs) may play an important role in the development of diabetic vascular sequelae. An AGE cross-link, pentosidine, is a sensitive and specific marker for tissue levels of AGEs. OBJECTIVES: To evaluate the role of AGEs in the development of diabetic nephropathy and retinopathy, we studied pentosidine levels and
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11. Advanced glycation end products contribute to amyloidosis in Alzheimer disease.
Alzheimer disease (AD) is characterized by deposits of an aggregated 42-amino-acid beta-amyloid peptide (beta AP) in the brain and cerebrovasculature. After a concentration-dependent lag period during in vitro incubations, soluble preparations of synthetic beta AP slowly form fibrillar aggregates that resemble natural amyloid and are measurable by sedimentat
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12. Receptor-specific increase in extracellular matrix production in mouse mesangial cells by advanced glycosylation end products is mediated via platelet-derived growth factor.
Renal disease is one of the most common and severe complications of diabetes mellitus. The hallmark of the disease, glomerulosclerosis, is characterized by an accumulation of extracellular matrix in the mesangial areas, leading to progressive obliteration of the vascular spaces. The role of the metabolic derangements of diabetes mellitus in the development o