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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.

Inflammatory markers are elevated in type 2 diabetic patients (DP) and may predict the development of type 2 diabetes. Our aims were to analyze differences in the expression of inflammatory and immunological molecules between DP and healthy subjects and to investigate whether glycemic control might prevent the overexpression of inflammatory markers in DP. Twenty-two DP with advanced atherosclerosis and eight healthy blood donors were included. DP were classified as well (HbA1c ≤ 6.5) or poorly controlled (HbA1c > 6.5). In "in vitro" studies, monocytes were exposed to low (5.5 mM) or high glucose (26 mM) concentrations in the absence or presence of insulin. Expression profiling of 14 inflammatory genes was analyzed using TLDA analysis. "In vivo" results show that monocytes from DP had increased levels of monocyte chemoattractant protein (MCP-1) and interleukin 6 (IL6) and lower levels of Toll-like receptor 2 (TLR2) mRNA than healthy subjects. Well-controlled DP had lower levels of IL-6 than poorly controlled DP, suggesting that glycemic control may prevent IL6 mRNA alterations associated with diabetes. "In vitro" results demonstrate that glucose directly and significantly induced MCP-1 and IL6 and reduced TLR2 mRNA expression. Insulin at high dose (100 IU/ml) dramatically enhanced the upregulatory effects of glucose on MCP-1 and IL-6 and reduced per se TLR2 mRNA expression. MCP-1, IL-6 and TLR2 are key inflammatory players altered in monocytes from type 2 DP. Both hyperinsulinemia and hyperglycemia contribute to alter the expression of these genes. The glycemic control only significantly prevented IL6 overexpression in this group of patients.