Sabina Galiniak, Grzegorz Bartosz, Izabela Sadowska-Bartosz

Galiniak, Sabina; Bartosz, Grzegorz; Sadowska-Bartosz, Izabela

doi:10.4149/gpb_2016044

Cited by 4 publications

(1 citation statement)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Advanced glycation end products (AGEs) are generated nonenzymatically, and the formation of AGEs is greatly accelerated by prolonged hyperglycemia in patients with diabetes mellitus (DM) [ 1 , 2 ]. AGE accumulation is one of the main factors that contribute to ageing and is an important element of etiopathology of age-related diseases, especially type 2 DM and its complications [ 3 – 5 ]. Recent studies have pointed out that AGE accumulation directly causes insulin-producing β -cell dysfunction and apoptosis in vivo [ 6 – 9 ].…”

Section: Introductionmentioning

confidence: 99%

Activation of NLRP3 Inflammasome by Advanced Glycation End Products Promotes Pancreatic Islet Damage

Kong

Yao

et al. 2017

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Accumulation of advanced glycation end products (AGEs) contributes to ageing and age-related diseases, especially type 2 diabetes. The NLRP3 inflammasome, as a vital component of the innate immune system, is implicated in the pathogenesis of type 2 diabetes. However, the role of the NLRP3 inflammasome in AGE-induced pancreatic islet damage remains largely unclear. Results showed that administration of AGEs (120 mg/kg for 6 weeks) in C57BL/6J mice induced an abnormal response to glucose (as measured by glucose tolerance and insulin release), pancreatic β-cell ultrastructural lesion, and cell death. These effects were associated with an excessive superoxide anion level, significant increased protein expression levels for NADPH oxidase 2 (NOX2), thioredoxin-interacting protein (TXNIP), NLRP3, and cleaved IL-1β, enhanced caspase-1 activity, and a significant increase in the levels of TXNIP–NLRP3 protein interaction. Ablation of the NLRP3 inflammasome or treatment with antioxidant N-acetyl-cysteine (NAC) clearly ameliorated these effects. In conclusion, our results reveal a possible mechanism for AGE-induced pancreatic islet damage upon NLRP3 inflammasome activation.

show abstract

Section: Introductionmentioning

confidence: 99%

Activation of NLRP3 Inflammasome by Advanced Glycation End Products Promotes Pancreatic Islet Damage

Kong

Yao

et al. 2017

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

pH-bioresponsive poly(ε-caprolactone)-based polymersome for effective drug delivery in cancer and protein glycoxidation prevention

Ghorbanizamani

Moulahoum

Sanli

et al. 2020

Archives of Biochemistry and Biophysics

View full text Add to dashboard Cite

High Plasmatic Levels of Advanced Glycation End Products are Associated with Metabolic Alterations and Insulin Resistance in Preeclamptic Women

García-Gómez

Bobadilla-Bravo

Díaz-Díaz

et al. 2021

CMM

View full text Add to dashboard Cite

Aims: The purpose of this study was to investigate the association between plasmatic levels of advanced end glycation products (AGEs) and the metabolic profile in subjects diagnosed with preeclampsia, due to the known relation of these molecules with oxidative stress and inflammation, which in turn are related with PE pathogenesis. Background: It has been reported that increased levels of AGEs are observed in patients with preeclampsia as compared with healthy pregnant subjects, which was mainly associated with oxidative stress and inflammation. Besides, in women with preeclampsia, there are metabolic changes such as hyperinsulinemia, glucose intolerance, dyslipidemia, among others, that are associated with an exacerbated insulin resistance. Additionally, some parameters indicate the alteration of hepatic function, such as increased levels of liver enzymes. However, the relationship of levels of AGEs with altered lipidic, hepatic and glucose metabolism parameters in preeclampsia has not been evaluated. Objective: To investigate the association between plasmatic levels of AGEs and hepatic, lipid and metabolic profiles in women diagnosed with preeclampsia. Methods: Plasma levels of AGEs were determined by a competitive enzyme-linked immunosorbent assay (ELISA) in 15 patients diagnosed with preeclampsia and 28 normoevolutive pregnant subjects (control group). Hepatic (serum creatinine, gamma-glutamyl transpeptidase, aspartate transaminase, alanine transaminase, uric acid, and lactate dehydrogenase), lipid (apolipoprotein A, apolipoprotein B, total cholesterol, triglycerides, low-density lipoproteins, and high-density lipoproteins) and metabolic variables (glucose, insulin, and insulin resistance) were assessed. Results: Plasmatic levels of AGEs were significantly higher in patients with preeclampsia as compared with the control. A positive correlation between circulating levels of AGEs and gamma-glutamyl transpeptidase, uric acid, glucose, insulin, and HOMA-IR levels was found in patients with preeclampsia. In conclusion, circulating levels of AGEs were higher in patients with preeclampsia than those observed in healthy pregnant subjects. Besides, variables of hepatic and metabolic profile, particularly those related to insulin resistance, were higher in preeclampsia as compared with healthy pregnant subjects. Interestingly, there is a positive correlation between AGEs levels and insulin resistance. Conclusions: Circulating levels of AGEs were higher in patients with preeclampsia than those observed in healthy pregnant subjects. Besides, hepatic and metabolic profiles, particularly those related to insulin resistance, were higher in preeclampsia as compared with healthy pregnant subjects. Interestingly, there is a positive correlation between AGEs levels and insulin resistance, suggesting that excessive glycation and an impaired metabolic profile contribute to the physiopathology of preeclampsia.

show abstract

Sabina Galiniak, Grzegorz Bartosz, Izabela Sadowska-Bartosz

Cited by 4 publications

References 45 publications

Activation of NLRP3 Inflammasome by Advanced Glycation End Products Promotes Pancreatic Islet Damage

Activation of NLRP3 Inflammasome by Advanced Glycation End Products Promotes Pancreatic Islet Damage

pH-bioresponsive poly(ε-caprolactone)-based polymersome for effective drug delivery in cancer and protein glycoxidation prevention

High Plasmatic Levels of Advanced Glycation End Products are Associated with Metabolic Alterations and Insulin Resistance in Preeclamptic Women

Contact Info

Product

Resources

About