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Therapeutic footwear (TFW) is essential to prevent diabetic foot ulcer (DFU) relapse after healing. Our retrospective study aimed at investigating patient's compliance with TFW 1 year after complete healing, and whether the respect of this TFW in real life conditions was associated with a decrease of DFU recurrence during a 1-year follow-up. This is a retrospective study in which all consecutive patients attending our ambulatory foot unit between 01.2015 and 01.2016, were included if they had a TFW prescription after complete healing. The primary study endpoint was the percentage of compliant patients, who wear the TFW at 1 year. The proportion of patient with DFU relapse was compared in compliant versus non-compliant patients (secondary endpoint). The use of TFW was assessed by analyzing the points of wear and cleanliness of the shoes by the same podiatrist. We included 117 consecutive patients: age 63 ± 13 years, women 29/117 (24,7%), type 2 diabetes: 108/117 (92%), diabetes duration: 17.5 ± 12.5 years. After 12 months, 28/117 patients (24%) were lost of follow-up. TFW was respected in 60/117 cases (51.2%). None of these factors influenced the TFW compliance: sex, age, type of diabetes, diabetic treatment, diabetic duration or complications, HbA1c level, peripheral artery disease, neuropathy, amputations, ulcer localization, healing time, TFW type nor the lack of social insurance. DFU recurrence was observed in 24/89 cases (27%) and was significantly higher in non-compliant patients: 16/29 (55%) vs. 8/60 (13.3%) (P=0.05). The only factor predictive of DFU relapse was non-compliance for TFW. After complete DFU healing, TFW prescription is respected only by half of the patients at 1 year. Non-compliant patients are at higher risk of DFU. Further surveys need to be designed to determine the reasons of non-compliance and to conceive more adapted educational programs. Disclosure: M. Laloi-Michelin: None. T. Vidal-Trécan: Board Member; Self; Novo Nordisk Inc. F. Féron: None. J. Kevorkian: None. D. Acker: None. C. Bouche: None. J. Gautier: None. J. Riveline: Board Member; Self; Abbott, Lilly Diabetes, Novo Nordisk Inc. Consultant; Self; Novo Nordisk Inc. Research Support; Self; Air Liquide, Amgen Inc. Speaker's Bureau; Self; Abbott, Lilly Diabetes, Sanofi. [ABSTRACT FROM AUTHOR]

The standard for measuring whole-body insulin sensitivity is via euglycemic-hyperinsulinemic clamp. In a given individual, it can vary significantly from hour to hour in response to interventions such as exercise, diet, drugs, and stressors. Over longer periods of time, fluctuations in body weight, physical activity, and progressive age, might alter insulin sensitivity. The variability of insulin sensitivity over time in persons at low risk for progression to diabetes is incompletely understood. We measured insulin sensitivities in 4 healthy volunteers with no family history of diabetes, 2M/2F, age 25±6y, BMI 22 ± 2 kg/m², FBS 90 ± 4 mg/dL, and A1c 5.0 ±0.2%. Each person was assessed 2-3 times over the course of 3.5 years via a 4-hour euglycemic-hyperinsulinemic clamp (2.0 mU/kg*min). Insulin levels were at steady-state during the fourth hour of the clamps as measured by RIA (173.6 ± 9.5 µU/mL). At this insulin level, hepatic glucose production is fully suppressed, so glucose utilization (M) was estimated by the glucose infusion rate, which initially was 11.6 ± 0.6 mg/kg*min. M did not change significantly over time, being 11.8 ± 1.2 mg/kg*min at the final evaluation. Over the study period, several metabolic indices varied substantially from the initial measurements in any given subject, with the following mean coefficients of variation (CV): BMI 4.9 ± 1.2%, FBS 4.4 ± 1.4%, fasting plasma insulin 45.0 ± 10.8%, HOMA-IR 46.9 ± 9.8%, total cholesterol 8.2 ± 3.1%, triglycerides 45.5 ± 6.0%, HDL 16.0 ± 5.8%, and LDL 16.4 ± 2.1%. We demonstrated a mean CV for M of 8.1 ± 0.2%. Since steady-state insulin levels achieved during the clamps also varied, we related whole-body insulin sensitivity to exogenous insulin via M/I* 100, whose cohort average at baseline was 14.6 ± 2.2 and at the end of the study 17.5 ± 1.9 (p=ns). The mean CV of the M/I* 100 for each of the subjects, over all of the clamps, was 12.2 ± 6.1%. By comparison, the initial and final HOMA-IR were, respectively, 1.1 ± 0.3 and 1.8 ± 0.4 (p=ns), and the mean CV over all measures was 55.1±13.3%. These results suggest a high degree of reproducibility of clamp-measured insulin sensitivity and that in healthy individuals at low risk for diabetes, insulin sensitivity does not change substantially or disproportionately to variations in other metabolic parameters over the course of several years. The considerably larger CV for HOMA-IR supports that it is not a robust index of insulin sensitivity when assessing individuals or smaller cohorts. [ABSTRACT FROM AUTHOR]

Oral hypoglycemic agents bind to the ATP-sensitive potassium channel and lower glucose levels effectively in individuals with diabetes. Although the principle mechanism of action can also promote hypoglycemia, clinically profound hypoglycemia is rare. Decreased stimulation of insulin secretion by these agents at mild hypoglycemia could provide protection from more profound hypoglycemia. Sulfonylureas and meglitinides bind to both shared and unique sites on the ATP-sensitive potassium receptor/channel complex but have different pharmacokinetic profiles. To evaluate the differential ability of both sulfonylureas and meglitinides to stimulate insulin release at modest hypoglycemia, we evaluated dextrose infusion rates necessary to maintain plasma glucose after oral administration of repaglinide (1 mg) or glipizide (5 mg) at euglycemia and again at modest hypoglycemia. Healthy subjects with no family history of diabetes underwent four clamp studies, two performed while maintaining isoglycemia (glucose levels at the fasted value) and two while maintaining modest hypoglycemia of 2.78 mmol/liter (50 mg/dl) induced by low-dose insulin infusion (3.6 pmol/kg.min). There was a marked decrease in the dextrose infusion rate with administration of either repaglinide or glipizide at hypoglycemia compared with drug administration at euglycemia (P