GW24-e1001 Effects of advanced glycation end products on function and angiogenesis of adipose tissue-derived stem cells and protective effects of Danhong injection

Heart ◽  
2013 ◽  
Vol 99 (Suppl 3) ◽  
pp. A30.2-A30
Author(s):  
Wu Feng ◽  
He Zhiqing ◽  
Ji Ruizhen ◽  
Wang Xin ◽  
Wu Zonggui ◽  
...  
Keyword(s):  
Stem Cells ◽  
Adipose Tissue ◽  
Advanced Glycation End Products ◽  
Protective Effects ◽  
Advanced Glycation ◽  
Danhong Injection ◽  
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

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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