scholarly journals Detection of Noncarboxymethyllysine and Carboxymethyllysine Advanced Glycation End Products (AGE) in Serum of Diabetic Patients

1999 ◽  
Vol 5 (6) ◽  
pp. 393-405 ◽  
Author(s):  
Masayoshi Takeuchi ◽  
Zenji Makita ◽  
Katsuyuki Yanagisawa ◽  
Yukihiko Kameda ◽  
Takao Koike
Keyword(s):  
Advanced Glycation End Products ◽  
Diabetic Patients ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals De Novo Hepatocellular Carcinoma in Hepatitis C-Related Cirrhosis: Are Advanced Glycation End Products a Key Driver?

2021 ◽  
Vol 11 ◽  
Author(s):  
Ahmed Abdel-Razik ◽  
Walaa Shabana ◽  
Ahmed Mohamed El Nakib ◽  
Mostafa Abdelsalam ◽  
Ahmed Abdelwahab ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Regression Analysis ◽  
Hepatitis C ◽  
Advanced Glycation End Products ◽  
Cox Regression ◽  
Diabetic Patients ◽  
Advanced Glycation ◽  
Cox Regression Analysis ◽  
Glycation End Products ◽  
End Products

Background and PurposeThe advanced glycation end products (AGEs) have been implicated in different diseases’ pathogenesis, but their role in hepatocellular carcinoma (HCC) is still a matter of debate. This study aims to investigate the association of AGEs with HCC development in patients with hepatitis C-related cirrhosis.MethodsOnly 153 of the 181 non-diabetic patients with cirrhosis were consecutively involved in this pilot cohort prospective study, along with 34 healthy control participants. Demographic characteristics, biochemical parameters, clinical data, and AGEs levels in all subjects at the starting point and every year after that for two years were assessed. Multivariable Cox regression analysis was used to settle variables that could predict HCC development within this period.ResultsHCC developed in 13 (8.5%) patients. Univariate Cox regression analysis reported that body mass index (P=0.013), homeostatic model assessment-insulin resistance (P=0.006), alpha-fetoprotein (P <0.001), and AGEs levels (P <0.001) were related to HCC development. After adjusting multiple confounders, the multivariable Cox regression model has revealed that AFP and AGEs were the powerful parameters related to the HCC occurrence (all P<0.05). AGEs at a cutoff value of more than 79.6 ng/ml had 100% sensitivity, 96.4% specificity, and 0.999 area under the curve (all P<0.001), using the receiver operating characteristic curve, for prediction of HCC development.ConclusionThis work suggests that AGEs are associated with an increased incidence of HCC, particularly in cirrhosis, which is encouraging in decreasing the risk of HCC in these patients.

Advanced glycation end-products associate with podocytopathy in type II diabetic patients

2021 ◽  
Author(s):  
Rajkishor Nishad ◽  
Tahaseen V Syed ◽  
Manga Motrapu ◽  
Rajesh Kavvuri ◽  
Kiranmayi Kodali ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Kidney Function ◽  
Advanced Glycation End Products ◽  
Diabetic Patients ◽  
Type Ii ◽  
Advanced Glycation ◽  
Mesenchymal Transition ◽  
Glycation End Products ◽  
End Products ◽  
Carboxymethyl Lysine

Abstract Background The prevalence of diabetes reaches epidemic proportions, affecting the incidence of diabetic nephropathy (DN) and associated end-stage kidney disease (ESKD). Diabetes is the leading cause of ESKD since 30–40% of diabetic patients develop DN. Albuminuria and eGFR have been considered a surrogate outcome of chronic kidney disease, and the search for a biomarker that predicts progression to diabetic kidney disease is intense.Methods We analyzed the association of serum advanced glycation end-products (AGEs) index (AGI) with impaired kidney function in uncontrolled diabetic patients (type II, n = 130) with albuminuria ranging from (150 to 450 mg/day). The kidney biopsy specimens were also examined for the association of AGEs, particularly carboxymethyl lysine (CML) with kidney function. Further, we also assessed the effect of carboxymethyl lysine on glomerular injury and podocytopathy in experimental animals.Results We observed a strong correlation between AGI and impaired kidney function in miroalbuminuric patients with hyperglycemia. A significant association between CML levels and impaired kidney function was noticed. Administration of CML in mice showed heavy proteinuria and glomerular abnormalities. Reduced podocyte number observed in mice administered with CML could be attributed to the epithelial-mesenchymal transition (EMT) of podocytes. Conclusion Serum AGEs could be independently related to the podocyte injury vis-a-vis the risk of DN progression to ESKD in patients with microalbuminuria. AGEs or CML could be considered a prognostic marker to assess microalbuminuria progression to ESKD in diabetic patients.

scholarly journals Advanced Glycation End-Products Suppress Mitochondrial Function and Proliferative Capacity of Achilles Tendon-Derived Fibroblasts

2019 ◽  
Author(s):  
Shivam H. Patel ◽  
Feng Yue ◽  
Shannon K. Saw ◽  
Rachel Foguth ◽  
Jason R. Cannon ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Achilles Tendon ◽  
Advanced Glycation End Products ◽  
Mitochondrial Function ◽  
Diabetic Patients ◽  
Proliferative Capacity ◽  
Advanced Glycation ◽  
Tendon Degeneration ◽  
Glycation End Products ◽  
End Products

AbstractDebilitating cases of tendon pain and degeneration affect the majority of diabetic individuals. The high rate of tendon degeneration persists even when glucose levels are well controlled, suggesting that other mechanisms may drive tendon degeneration in diabetic patients. The purpose of this study was to investigate the impact of advanced glycation end-products on tendon fibroblasts to further our mechanistic understanding of the development and progression of diabetic tendinopathy. We proposed that advanced glycation end-products would induce limitations to mitochondrial function and proliferative capacity in tendon-derived fibroblasts, restricting their ability to maintain biosynthesis of tendon extracellular matrix. Using an in-vitro cell culture system, rat Achilles tendon fibroblasts were treated with glycolaldehyde-derived advanced glycation end-products (0, 50, 100, and 200μg/ml) for 48 hours in normal glucose (5.5mM) and high glucose (25mM) conditions. We demonstrate that tendon fibroblasts treated with advanced glycation end-products display reduced ATP production, electron transport efficiency, and proliferative capacity. These impairments were coupled with alterations in mitochondrial DNA content and expression of genes associated with extracellular matrix remodeling, mitochondrial energy metabolism, and apoptosis. Our findings suggest that advanced glycation end-products disrupt tendon fibroblast homeostasis and may be involved in the development and progression of diabetic tendinopathy.

scholarly journals Advanced Glycation end product profile of Diabetic and Non-Diabetic patients with cataract

2021 ◽  
pp. 14-20
Author(s):  
Emma-Okon B.O ◽  
Onakpoya O.H ◽  
Kolawole B.A ◽  
Owolabi F.A ◽  
Akinde M.O ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Lipid Peroxidation ◽  
Advanced Glycation End Products ◽  
Fasting Blood Glucose ◽  
Diabetic Patients ◽  
Healthy Controls ◽  
Reaction Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

The study determined the levels of advanced glycation end-products (AGEs) and malondialdehyde (MDA) in Nigerian cataract patients with and without diabetes mellitus, those with DM but no cataract as well as apparently healthy controls with a view to further elucidating putative pathophysiologic mechanisms for the occurrence of cataracts among our diabetic population. Participants comprised of 30 diabetic patients with operable cataract, 30 non-diabetic patients with operable cataract, 30 diabetic patients without cataract and 17 healthy controls all matched for age and sex, Glycated Haemoglobin levels in whole blood samples were determined using an affinity assay while fasting blood glucose was estimated by the glucose oxidase reaction. AGE was measured using a competitive ELISA kit while the level of lipid peroxidation in plasma was determined by measuring the reaction products between malondialdehyde and thiobarbituric acid. Statistical analysis was carried out using SPSS software (version 23). P<0.05 was taken as significant. The age range of participants was 52-90 years with a mean of 67.2±0.8. Mean levels of AGE were comparable in patients who had diabetes and cataract, those with cataract but no diabetes and those with Diabetes but no cataracts while healthy controls of similar age group had significantly lower levels. Patients with diabetes mellitus and cataract had significantly higher levels of MDA than those with diabetes only. There was positive, significant correlation between AGE and fasting glucose levels. No significant differences existed between AGE and MDA levels in male and female respondents. We conclude that AGE may serve as a useful index of pathologic conditions, including cataract and diabetes. Keywords: Advanced Glycation End-Products; Cataract; Diabetes; Lipid Peroxidation

scholarly journals Advanced Glycation End Products (AGEs), Receptor for AGEs, Diabetes, and Bone: Review of the Literature

2019 ◽  
Vol 3 (10) ◽  
pp. 1799-1818 ◽  
Author(s):  
Kamyar Asadipooya ◽  
Edilfavia Mae Uy
Keyword(s):  
Signaling Pathway ◽  
Advanced Glycation End Products ◽  
Cell Metabolism ◽  
Bone Cell ◽  
Diabetic Patients ◽  
Advanced Glycation ◽  
Soluble Rage ◽  
Increased Risk ◽  
Glycation End Products ◽  
End Products

AbstractDiabetes compromises bone cell metabolism and function, resulting in increased risk of fragility fracture. Advanced glycation end products (AGEs) interact with the receptor for AGEs (RAGE) and can make a meaningful contribution to bone cell metabolism and/or alter function. Searches in PubMed using the key words “advanced glycation end-product,” “RAGE,” “sRAGE,” “bone,” and “diabetes” were made to explain some of the clinical outcomes of diabetes in bone metabolism through the AGE–RAGE signaling pathway. All published clinical studies were included in tables. The AGE–RAGE signaling pathway participates in diabetic complications, including diabetic osteopathy. Some clinical results in diabetic patients, such as reduced bone density, suppressed bone turnover markers, and bone quality impairment, could be potentially due to AGE–RAGE signaling consequences. However, the AGE–RAGE signaling pathway has some helpful roles in the bone, including an increase in osteogenic function. Soluble RAGE (sRAGE), as a ligand decoy, may increase in either conditions of RAGE production or destruction, and then it cannot always reflect the AGE–RAGE signaling. Recombinant sRAGE can block the AGE–RAGE signaling pathway but is associated with some limitations, such as accessibility to AGEs, an increase in other RAGE ligands, and a long half-life (24 hours), which is associated with losing the beneficial effect of AGE/RAGE. As a result, sRAGE is not a helpful marker to assess activity of the RAGE signaling pathway. The recombinant sRAGE cannot be translated into clinical practice due to its limitations.

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