The mechanism(s) resulting in the premature atherosclerosis of diabetes is unknown. Increased phagocyte release of reactive oxygen species such as superoxide anion (O2(·-)), resulting in low-density lipoprotein (LDL) oxidation, could be one possible cause. The purpose of the present study was to compare the abilities of polymorphonuclear leukocytes (PMN) from 12 non-insulin-dependent diabetes mellitus (NIDDM) subjects free of vascular disease to produce O2(·-) anion and oxidize LDL with PMN from age- and gender-matched normoglycemic controls. PMN were activated with phorbol 12-myristate 13-acetate (PMA) to measure O2(·-) production. In addition, the PMN were activated with PMA and opsonized zymosan (OZ) to assess LDL oxidation over 5 hours. LDL oxidation was measured by conjugated diene formation and apolipoprotein B (apo B) fluorescence, PMN superoxide production stimulated by PMA was similar between groups. LDL oxidation by PMN was also not different between the NIDDM and control groups. The results of this study indicate that PMN O2(·-) production and LDL oxidation are not enhanced in NIDDM subjects without: vascular disease. Other factors, such as reduced antioxidant concentrations and non-enzymatic glycation of LDL, may play a greater role in the premature atherosclerosis of diabetes.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism