AIM: To investigate whether levels of blood HbA1c in diabetic patients are associated with susceptibility of LDL to oxidation. METHODS: LDL was separated from blood of 40 diabetic patients with known blood glucose and HbA1c levels. The tendency to undergo lipid peroxidation was assessed via lag time required for initiation of LDL oxidation. HbA1c formation was measured in vitro following incubation of red blood cell (RBC) hemolysate for 3 months with increasing concentrations of glucose in the absence or presence of LDL or oxidized LDL. RESULTS: Lag time for copper-induced LDL oxidation was twice as long in normal subjects compared to diabetic patients. Correlation analyses between LDL oxidation lag time and HbA1c blood levels revealed an R value of 0.74. Incubation of RBC hemolysate with high glucose concentration (up to 400 mg/dl) resulted in increased blood HbA1c concentration by up to 107%. Addition of LDL to this hemolysate over a period of 3 months resulted in LDL oxidation and an increase in HbA1c levels by up to 168%. Similarly, addition of oxidized LDL to the hemolysate increased HbA1c by up to 240%. CONCLUSIONS: Increased tendency of LDL to undergo lipid peroxidation in diabetic patients contributes to increased levels of blood HbA1c, mainly in those with HbA1c<7.3.
AIM: To investigate whether levels of blood HbA1c in diabeticpatients are associated with susceptibility of LDL to oxidation. METHODS: LDL was separated from blood of 40 diabeticpatients with known blood glucose and HbA1c levels. The tendency to undergo lipid peroxidation was assessed via lag time required for initiation of LDL oxidation. HbA1c formation was measured in vitro following incubation of red blood cell (RBC) hemolysate for 3 months with increasing concentrations of glucose in the absence or presence of LDL or oxidized LDL. RESULTS: Lag time for copper-induced LDL oxidation was twice as long in normal subjects compared to diabeticpatients. Correlation analyses between LDL oxidation lag time and HbA1c blood levels revealed an R value of 0.74. Incubation of RBC hemolysate with high glucose concentration (up to 400 mg/dl) resulted in increased blood HbA1c concentration by up to 107%. Addition of LDL to this hemolysate over a period of 3 months resulted in LDL oxidation and an increase in HbA1c levels by up to 168%. Similarly, addition of oxidized LDL to the hemolysate increased HbA1c by up to 240%. CONCLUSIONS: Increased tendency of LDL to undergo lipid peroxidation in diabeticpatients contributes to increased levels of blood HbA1c, mainly in those with HbA1c<7.3.
Authors: Alliny de Souza Bastos; Dana T Graves; Ana Paula de Melo Loureiro; Carlos Rossa Júnior; Sâmia Cruz Tfaile Corbi; Fausto Frizzera; Raquel Mantuaneli Scarel-Caminaga; Niels Olsen Câmara; Oelisoa M Andriankaja; Meire I Hiyane; Silvana Regina Perez Orrico Journal: J Diabetes Complications Date: 2016-07-21 Impact factor: 2.852
Authors: Timothy C Nichols; Elizabeth P Merricks; Dwight A Bellinger; Robin A Raymer; Jing Yu; Diana Lam; Gary G Koch; Walker H Busby; David R Clemmons Journal: PLoS One Date: 2015-07-06 Impact factor: 3.240