Serum albumin modified by carbamoylation impairs macrophage cholesterol efflux in diabetic kidney disease

Abnormalities in lipid metabolism, accumulation of uremic toxins and advanced glycation end products may contribute to worsening atherosclerosis. This study characterized the glycation and carbamoylation profile of serum albumin isolated from individuals with diabetic kidney disease and its influenc...

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Veröffentlicht in:Journal of diabetes and its complications 2021-09, Vol.35 (9), p.107969-107969, Article 107969
Hauptverfasser: de Araújo Lira, Aécio Lopes, de Fátima Mello Santana, Monique, de Souza Pinto, Raphael, Minanni, Carlos André, Iborra, Rodrigo Tallada, de Lima, Adriana Machado Saldiba, Correa-Giannella, Maria Lúcia, Passarelli, Marisa, Queiroz, Márcia Silva
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Sprache:eng
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Zusammenfassung:Abnormalities in lipid metabolism, accumulation of uremic toxins and advanced glycation end products may contribute to worsening atherosclerosis. This study characterized the glycation and carbamoylation profile of serum albumin isolated from individuals with diabetic kidney disease and its influence on cholesterol efflux. 49 patients with type 2 diabetes (T2DM) and different eGFR evaluated glycation and carbamoylation profile by measurement of carboxymethyl lysine (CML) and carbamoylated proteins (CBL) in plasma by ELISA, homocitrulline (HCit) in plasma by colorimetry. In the isolated albumins, we quantified CBL (ELISA) and total AGE and pentosidine by fluorescence. Macrophages were treated with albumin isolated, and 14C-Cholesterol efflux mediated by HDL2 or HDL3 was measured. Kruskal-Wallis test, Jonckheere-Terpstra test and Brunner's posttest were used for comparisons among groups. Determination of CML, HCit, CBL in plasma, as total AGE and pentosidine in albumins, did not differ between groups; however, CBL in the isolated albumins was higher in the more advanced stages of CKD (p=0.0414). There was reduction in the 14C-cholesterol efflux after treatment for 18h with albumin isolated from patients with eGFR
ISSN:1056-8727
1873-460X
DOI:10.1016/j.jdiacomp.2021.107969