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CD36 overexpression: a possible etiopathogenic mechanism of atherosclerosis in patients with prediabetes and diabetes

RATIONALE: CD36 is a scavenger receptor located on monocytes which is involved in foam cell transformation. AIM: To evaluate CD36 expression under different glycemic states in both healthy subjects and in atherosclerotic patients. SUBJECTS AND METHODS: In order to evaluate the possible effects of hy...

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Detalles Bibliográficos
Autores principales: Lopez-Carmona, M. D., Plaza-Seron, M. C., Vargas-Candela, A., Tinahones, F. J., Gomez-Huelgas, R., Bernal-Lopez, M. R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5516302/
https://www.ncbi.nlm.nih.gov/pubmed/28729885
http://dx.doi.org/10.1186/s13098-017-0253-x
Descripción
Sumario:RATIONALE: CD36 is a scavenger receptor located on monocytes which is involved in foam cell transformation. AIM: To evaluate CD36 expression under different glycemic states in both healthy subjects and in atherosclerotic patients. SUBJECTS AND METHODS: In order to evaluate the possible effects of hyperglycemia on CD36 expression in healthy subjects, an in vitro experiment was carried out using monocyte in three different conditions: extreme hyperglycemia (HG), euglycemia (EG) and in the absence of glucose. On the other hand, three groups of atherosclerotic patients were evaluated according to their glycemic conditions: normoglycemic (NG), prediabetic (preDM) and diabetic (DM) patients. CD36 expression (mRNA, non-glycated and glycated protein) was analyzed in monocytes. RESULTS: CD36 mRNA expression in the in vitro experiment peaked at 4 and 24 h under HG conditions. No differences in mRNA levels were found in the EG and control group. The level of non-glycated proteins was higher in HG and EG conditions compared with control group. Glycated protein expression was inhibited by glucose in a sustained manner. In atherosclerotic patients, a significant association was observed when comparing glycated CD36 protein expression in DM with NG patients (p = 0.03). No significant differences were found in mRNA and non-glycated CD36 expression in these patients. Moreover, BMI, insulin, weight and treatment were shown to be related to CD36 expression (mRNA, non-glycated and glycated protein levels, depending of the case) in atherosclerotic patients. CONCLUSIONS: Hyperglycemia is an important modulator of CD36 mRNA and non-glycated protein expression in vitro, increasing de novo synthesis in healthy subjects. In atherosclerotic patients, there are progressive increases in CD36 receptors, which may be due to a post-translational stimulus.