Interplay of Dinner Timing and MTNR1B Type 2 Diabetes Risk Variant on Glucose Tolerance and Insulin Secretion: A Randomized Crossover Trial.

OBJECTIVE: We tested whether the concurrence of food intake and elevated concentrations of endogenous melatonin, as occurs with late eating, results in impaired glucose control, in particular in carriers of the type 2 diabetes-associated G allele in the melatonin receptor-1B gene (MTNR1B). RESEARCH DESIGN AND METHODS: In a Spanish natural late-eating population, a randomized, crossover study was performed. Each participant (n = 845) underwent two evening 2-h 75-g oral glucose tolerance tests following an 8-h fast: an early condition scheduled 4 h prior to habitual bedtime ("early dinner timing") and a late condition scheduled 1 h prior to habitual bedtime ("late dinner timing"), simulating an early and a late dinner timing, respectively. Differences in postprandial glucose and insulin responses between early and late dinner timing were determined using incremental area under the curve (AUC) calculated by the trapezoidal method. RESULTS: Melatonin serum levels were 3.5-fold higher in the late versus early condition, with late dinner timing resulting in 6.7% lower insulin AUC and 8.3% higher glucose AUC. The effect of late eating impairing glucose tolerance was stronger in the MTNR1B G-allele carriers than in noncarriers. Genotype differences in glucose tolerance were attributed to reductions in ß-cell function (P for interaction, Pint glucose area under the curve = 0.009, Pint corrected insulin response = 0.022, and Pint disposition index = 0.018). CONCLUSIONS: Concurrently high endogenous melatonin and carbohydrate intake, as typical for late eating, impairs glucose tolerance, especially in MTNR1B G-risk allele carriers, attributable to insulin secretion defects.

Prevalence of bacterial contamination of glucose test strips in individual single-use packets versus multiple-use vials.

BACKGROUND: Glucose measurement is the cornerstone of diabetes control. In the hospital setting, the same device and package of test strips (50 or 100 strips) can be used to monitor glucose in several patients, which can increase cross contamination. The objective of our study is to measure bacterial contamination in glucose test strips, comparing results in individual single-use packets (one hospital) versus multi-use vials (two hospitals) in Spain. METHODS: Test strips were collected from five different wards. Each hospital also collected two unopened vials from a single ward as controls. They were sent to a reference laboratory for microbiologic study. A number equal or higher than two colony forming units per strip was considered as a positive result. RESULTS: Out of 423 glucose test strips collected and cultured, 146 were contaminated (34%); only 7% of individually packed strips were contaminated versus 45% of strips packed in multi-use vials, with a high statistical significance (p < .001). CONCLUSIONS: In the strips from multi-use vials, a high contamination rate was found and highly pathogenic organisms were identified, such as methicillin-resistant Staphylococcus epidermidis or Staphylococcus hemolyticus. In contrast, in strips packed individually, there was a much lower contamination rate and no such pathogen organisms were found. Therefore, in the hospital setting, the use of blood glucose test strips in individual packages would be more advantageous (mainly from a clinical point of view, but also from a financial one) than those packed in multi-use vials.