TY - JOUR
T1 - Increased inflammatory effect of electronegative LDL and decreased protection by HDL in type 2 diabetic patients
AU - Estruch, Montserrat
AU - Miñambres, Inka
AU - Sanchez-Quesada, Jose Luis
AU - Soler, Marta
AU - Pérez, Antonio
AU - Ordoñez-Llanos, Jordi
AU - Benitez, Sonia
N1 - Copyright © 2017 Elsevier B.V. All rights reserved.
PY - 2017/10
Y1 - 2017/10
N2 - BACKGROUND AND AIMS: Type 2 diabetic patients have an increased proportion of electronegative low-density lipoprotein (LDL(-)), an inflammatory LDL subfraction present in blood, and dysfunctional high-density lipoprotein (HDL). We aimed at examining the inflammatory effect of LDL(-) on monocytes and the counteracting effect of HDL in the context of type 2 diabetes.METHODS: This was a cross-sectional study in which the population comprised 3 groups (n = 12 in each group): type 2 diabetic patients with good glycaemic control (GC-T2DM patients), type 2 diabetic patients with poor glycaemic control (PC-T2DM), and a control group. Total LDL, HDL, and monocytes were isolated from plasma of these subjects. LDL(-) was isolated from total LDL by anion-exchange chromatography. LDL(-) from the three groups of subjects was added to monocytes in the presence or absence of HDL, and cytokines released by monocytes were quantified by ELISA.RESULTS: LDL(-) proportion and plasma inflammatory markers were increased in PC-T2DM patients. LDL(-) from PC-T2DM patients induced the highest IL1β, IL6, and IL10 release in monocytes compared to LDL(-) from GC-T2DM and healthy subjects, and presented the highest content of non-esterified fatty acids (NEFA). In turn, HDL from PC-T2DM patients showed the lowest ability to inhibit LDL(-)-induced cytokine release in parallel to an impaired ability to decrease NEFA content in LDL(-).CONCLUSIONS: Our findings show an imbalance in the pro- and anti-inflammatory effects of lipoproteins from T2DM patients, particularly in PC-T2DM.
AB - BACKGROUND AND AIMS: Type 2 diabetic patients have an increased proportion of electronegative low-density lipoprotein (LDL(-)), an inflammatory LDL subfraction present in blood, and dysfunctional high-density lipoprotein (HDL). We aimed at examining the inflammatory effect of LDL(-) on monocytes and the counteracting effect of HDL in the context of type 2 diabetes.METHODS: This was a cross-sectional study in which the population comprised 3 groups (n = 12 in each group): type 2 diabetic patients with good glycaemic control (GC-T2DM patients), type 2 diabetic patients with poor glycaemic control (PC-T2DM), and a control group. Total LDL, HDL, and monocytes were isolated from plasma of these subjects. LDL(-) was isolated from total LDL by anion-exchange chromatography. LDL(-) from the three groups of subjects was added to monocytes in the presence or absence of HDL, and cytokines released by monocytes were quantified by ELISA.RESULTS: LDL(-) proportion and plasma inflammatory markers were increased in PC-T2DM patients. LDL(-) from PC-T2DM patients induced the highest IL1β, IL6, and IL10 release in monocytes compared to LDL(-) from GC-T2DM and healthy subjects, and presented the highest content of non-esterified fatty acids (NEFA). In turn, HDL from PC-T2DM patients showed the lowest ability to inhibit LDL(-)-induced cytokine release in parallel to an impaired ability to decrease NEFA content in LDL(-).CONCLUSIONS: Our findings show an imbalance in the pro- and anti-inflammatory effects of lipoproteins from T2DM patients, particularly in PC-T2DM.
KW - Cross-Sectional Studies
KW - Diabetes Mellitus, Type 2/blood
KW - Humans
KW - Inflammation/etiology
KW - Lipoproteins, HDL/physiology
KW - Lipoproteins, LDL/physiology
KW - Monocytes/physiology
U2 - 10.1016/j.atherosclerosis.2017.07.015
DO - 10.1016/j.atherosclerosis.2017.07.015
M3 - Journal article
C2 - 28734591
SN - 1567-5688
VL - 265
SP - 292
EP - 298
JO - Atherosclerosis
JF - Atherosclerosis
ER -