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 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.

Assessment of an educational intervention in the management of non-critical inpatient glycemic control.

In hospitalized diabetic patients, the recommended insulin therapy is basal bolus plus correction-dose regimen instead of sliding-scale insulin. The purpose of this study was to evaluate the effect of the implementation of a new protocol based on basal bolus therapy on managing diabetes in a university hospital setting. We performed a cross-sectional study before and 12 months after a 4-month intervention period to implement a basal bolus regimen in hospitalized patients. Non-critical patients admitted into the hospital for at least 72 h were included. Changes in prescribing habits, glucose control and incidence of hypoglycemia were evaluated. An increase in the use of the new protocol and a decrease in sliding scale were observed after the intervention. In the pre-intervention group, a total of 59.2% glucose readings were between 70 and 180 mg/dL versus 57.1% after the intervention, without observing statistical differences. Significant reductions in hypoglycemia between pre- and post-intervention (13.04 vs. 4.08%, p = 0.0215) were observed. The percentage of hospitalized diabetic patients who had HbA1c was 10.43 and 4.08% in pre- and post-intervention phases, respectively. The protocol showed beneficial outcomes in terms of fewer hypoglycemia episodes and reflected a change in prescription habits, but it did not improve glycemic control. Furthermore, the percentage of patients who had an HbA1c test during their hospitalization remained very low after the intervention. This fact may seriously limit the correct management of hyperglycemia after the hospital discharge.