Diabetes research and clinical practice · 2020
Monocyte CD36 expression associates with atherosclerotic burden in diabetes mellitus.
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Chandran Jayanthi, Wadhwa Neelam, Madhu S V, Kumar Rajive, Sharma Satendra
Аннотация
BACKGROUND: By virtue of its role in oxidized low-density lipoprotein uptake and foam cell transformation, monocyte CD36 (mCD36) is a potential non-invasive tool to detect atherosclerosis (ATH) in patients of type 2 diabetes mellitus (DM).
METHODS: Flowcytometric expression of mCD36 was evaluated with reference to ankle brachial index (ABI) in 70 patients of type 2 DM [40 with and 30 without coronary artery disease (CAD) respectively] and 30 age and gender matched normoglycemic controls (NGCs).
RESULTS: DM patients had significantly higher mCD36 indices than NGCs (p < 0.001). The mCD36 expression was significantly higher in DM persons with CAD and those with poor glycemia control (glycosylated haemoglobin, HbA1c ≥ 7%) than their respective counterparts (p < 0.001 for both). Thirty subjects had compromised ABI (≤0.9); all were DM persons with CAD. ABI compromised subjects had consistently higher mCD36 indices than all other sub-groups (p < 0.001 for all comparisons). Notably, within the ABI-uncompromised group, mCD36 indices differed significantly and showed progressive increase from NGCs to diabetics without and with CAD respectively.
CONCLUSIONS: mCD36 plays an important role in atherogenesis. With reference to ABI, mCD36 performed robustly as a marker of ATH. Furthermore, it could stratify subjects within the 'ABI-uncompromised group' commensurate with their conventional clinico-pathological ATH risk predisposition.
METHODS: Flowcytometric expression of mCD36 was evaluated with reference to ankle brachial index (ABI) in 70 patients of type 2 DM [40 with and 30 without coronary artery disease (CAD) respectively] and 30 age and gender matched normoglycemic controls (NGCs).
RESULTS: DM patients had significantly higher mCD36 indices than NGCs (p < 0.001). The mCD36 expression was significantly higher in DM persons with CAD and those with poor glycemia control (glycosylated haemoglobin, HbA1c ≥ 7%) than their respective counterparts (p < 0.001 for both). Thirty subjects had compromised ABI (≤0.9); all were DM persons with CAD. ABI compromised subjects had consistently higher mCD36 indices than all other sub-groups (p < 0.001 for all comparisons). Notably, within the ABI-uncompromised group, mCD36 indices differed significantly and showed progressive increase from NGCs to diabetics without and with CAD respectively.
CONCLUSIONS: mCD36 plays an important role in atherogenesis. With reference to ABI, mCD36 performed robustly as a marker of ATH. Furthermore, it could stratify subjects within the 'ABI-uncompromised group' commensurate with their conventional clinico-pathological ATH risk predisposition.