GW24-e1002 Advanced glycation end products induces apoptosis and shorts telomere length in human adipose tissue-drived stem cells through modulation of MAPK pathways

Heart ◽  
2013 ◽  
Vol 99 (Suppl 3) ◽  
pp. A17.2-A18
Author(s):  
Wu Feng ◽  
He Zhiqing ◽  
Ji Ruizhen ◽  
Wang Xin ◽  
Wu Zonggui ◽  
...  
Keyword(s):  
Stem Cells ◽  
Adipose Tissue ◽  
Telomere Length ◽  
Advanced Glycation End Products ◽  
Human Adipose Tissue ◽  
Advanced Glycation ◽  
Mapk Pathways ◽  
Glycation End Products ◽  
End Products

Stem Cells in Head and Neck Cancers Pathogenesis: Are Advanced Glycation End Products (AGEs) Involved?

2018 ◽  
Vol 04 (02) ◽  
Author(s):  
Petrescu Bianca Nausica ◽  
Babtan Anida Maria ◽  
Soritau Olga ◽  
Buhate Dan ◽  
Ionel Anca ◽  
...  
Keyword(s):  
Stem Cells ◽  
Head And Neck ◽  
Advanced Glycation End Products ◽  
Head And Neck Cancers ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Shorter Telomere Length in Carriers of APOE-ε4 and High Plasma Concentration of Glucose, Glyoxal and Other Advanced Glycation End Products (AGEs)

2019 ◽  
Vol 75 (10) ◽  
pp. 1894-1898 ◽  
Author(s):  
Varinderpal S Dhillon ◽  
Permal Deo ◽  
Ann Chua ◽  
Phil Thomas ◽  
Michael Fenech
Keyword(s):  
Risk Factor ◽  
Telomere Length ◽  
Advanced Glycation End Products ◽  
Biological Aging ◽  
Advanced Glycation ◽  
Apoe Ε4 ◽  
Increased Risk ◽  
Glycation End Products ◽  
End Products ◽  
Ε4 Allele

Abstract Apolipoprotein-ε4 (APOE-ε4)—common variant is a major genetic risk factor for cognitive decline and Alzheimer's disease (AD). An accelerated rate of biological aging could contribute to this increased risk. Glycation of serum proteins due to excessive glucose and reactive oxygen species leads to the formation of advanced glycation end products (AGEs)—a risk factor for diabetes and AD, and decline in motor functioning in elderly adults. Aim of present study was to investigate impact of APOE-ε4 allele containing genotype and accumulation of AGEs in plasma on telomere length (TL). Results showed that TL is significantly shorter in APOE-ε4 carriers compared with non-APOE-ε4 carriers (p = .0003). Higher plasma glucose level was associated with shorter TL irrespective of APOE-ε4 allele containing genotype (r = −.26; p = .0004). With regard to AGEs, higher plasma glyoxal and fluorescent AGEs concentrations were inversely related to TL (r = −.16; p = .03; r = −.28; p = .0001), however, plasma Nε-(carboxymethyl)lysine levels didn't correlate with TL (r = −.04; p = .57). Results support the hypotheses that APOE-ε4 carriers have shorter telomeres than noncarriers and telomere erosion is increased with higher concentration of glucose, fluorescent AGEs, and glyoxal.

In vitro chronic glycation induces AGEs accumulation reducing insulin stimulated glucose uptake and increasing GLP1R in adipocytes

2021 ◽  
Author(s):  
Nino C Chilelli ◽  
Alessia Faggian ◽  
Francesca Favaretto ◽  
Gabriella Milan ◽  
Chiara Compagnin ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Advanced Glycation End Products ◽  
Glucose Transporter ◽  
Adipogenic Differentiation ◽  
Continuous Process ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Insulin Responsiveness

Glycation is one of the most important post-translational modifications in cells and tissues and gives rise to highly reactive species called advanced glycation end products (AGEs). AGEs exert their pathological effects through different ways and previous reports suggest that they may also affect adipose tissue function and insulin sensitivity. All the data belong only to short-term treatments; however, in vivo glycation is a continuous process. To fill this gap, our study investigated the effect of chronic pro-glycating conditions on adipogenesis and adipocyte's insulin responsiveness. Our results show that chronic pro-glycating treatments with methylglyoxal (MGO) and MGO modified-BSA (BSA-MGO) do not display cytotoxicity but modify gene expression without affect adipogenic differentiation. These treatments induce different levels of intracellular accumulation of AGEs which colocalize with the insulin-sensitive glucose transporter GLUT4 (solute carrier family 2 member 4- SLC2A4) in the cytoplasm; in particular, BSA-MGO reduces glucose uptake. Moreover, the adipocytes differentiated in pro-glycating conditions display an enhancement in the protein expression of the receptor for advanced glycation end products (RAGE) and glucagon-like peptide 1 receptor (GLP1R). These results suggest that intracellular AGEs could link alterations in GLP1 signaling and insulin resistance in adipose tissue, revealing that GLUT4 protein can be susceptible to glycation. Further studies are needed to clarify if this pathway could be targeted and if the reduction of AGEs accumulation in adipocytes can ameliorate insulin responsiveness.

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