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Clinically acceptable user proficiency in capillary blood glucose testing can be maintained in most subjects, with recurrent intensive education during follow-up clinic visits. Therefore, we recommend that these comparisons be performed and patient's technique be observed at each visit to monitor their performance. The clinic glucose meter is a suitable alternative to a clinical laboratory for user proficiency checks.

By lowering the daily insulin dose, sulfonylurea drugs appear to improve the sensitivity of exogenous insulin in subjects with type 2 diabetes mellitus manifesting lapse of glycemic control. Moreover, glimepiride appears to possess a greater insulin-sparing property than other sulfonylureas.

Background: Lack of first phase insulin secretion during oral glucose tolerance test [OGTT] in Type 2 Diabetes Mellitus (DM) is attributed to glucose toxicity. Alternatively, the role of insulin resistance in impaired insulin release secondary to lack of glucose entry into β cells may be responsible, but is not examined. Aim: The role of insulin sensitivity in 1st phase insulin secretion was assessed. Material and Methods: Plasma glucose (G) and insulin (I) concentrations were determined after an overnight fast (F) and upto 60 minutes during OGTT with glucose 75g in 12 normal (N), 14 with impaired glucose tolerance (IGT) and 41 subjects with Type 2 DM. First phase insulin secretion (Δ Insulin) was determined as a percentage rise from baseline 100x (Peak-Basal)/Basal. Insulin sensitivity was determined as FI x FG (mUxmM/L). Results: FG were normal (< 5.5 mM/L) in both N and IGT; and >7.0 mM/L in Type 2 DM. FI x FG and ? insulin were 35 ± 4 and 389 ± 89% in N; 77 ± 5 and 254 ± 65% in IGT; and 235 ± 19 and 95 ± 15% in Type 2 DM. Significant negative correlations were noted between ? insulin one hand and FI x FG on the other amongst all subjects [p < 0.0001 for all correlations]. Conclusion: Decline of 1st phase insulin secretion in IGT and Type 2 DM may be attributed to inhibited release of depleted insulin stores in the β Cells induced by impaired glucose entry due to insulin resistance, and is unlikely to be caused by glucose toxicity in IGT in presence of fasting euglycemia