Results for HbA1c (A), severe or BG-confirmed symptomatic hypoglycemia (B), change in body weight (C), daily total insulin dose (D), FPG (E), and nine-point.

Slides:

Advertisements

Similar presentations

New Insulin Glargine 300 Units/mL Versus Glargine 100 Units/mL in People With Type 2 Diabetes Using Basal and Mealtime Insulin: Glucose Control and Hypoglycemia.

Advertisements

Contrasting Effects of Lixisenatide and Liraglutide on Postprandial Glycemic Control, Gastric Emptying, and Safety Parameters in Patients With Type 2 Diabetes.

New Insulin Formulations Guillermo Umpierrez, MD, FACP, FACE Professor of Medicine Emory University School of Medicine Part 1.

Contributions to Type 2 Diabetes. Glucose in balance meal Time in minutes Blood glucose levels, mg/dL Insulin levels, uU/mL Glucagon.

Adding Once-Daily Lixisenatide for Type 2 Diabetes Inadequately Controlled With Newly Initiated and Continuously Titrated Basal Insulin Glargine A 24-Week,

Introduction Subcutaneous insulin absorption is not reproducible and insulin entry directly into the circulation is not linked to glucose sensing Basal.

Achieving Optimal Glycaemic Control: Can Insulin Deliver?

Key publication slides

Insulin and Incretins: the perfect Partnership?

Neal B, et al. Diabetes Care 2015;38:403–411

Insulin glargine compared with premixed insulin for management of insulin-naïve type 2 diabetes patients uncontrolled on oral antidiabetic drugs: the.

with undiagnosed diabetes mellitus by three diagnostic criteria

Insulin Intensification Strategies in Later-Stage Type 2 Diabetes Mellitus.

Key clinical efficacy outcomes for (A) hemoglobin A1c (HbA1c), (B) weight change. Key clinical efficacy outcomes for (A) hemoglobin A1c (HbA1c), (B) weight.

A: Percentage of type 1 diabetic and type 2 diabetic patients with asymptomatic hypoglycemias detected by the CGMS. B: Daily distribution of asymptomatic.

Novel Insulin Combinations: What Does the Primary Care Physician Need to Know?

Distribution of the absolute percentage differences of each basal rate estimate to final basal rates. Distribution of the absolute percentage differences.

Selected efficacy and safety parameters.

Key Insulin Side Effects*

Frequency of potential risk of hypoglycemia for each estimate method, defined as a percentage difference between the estimate and final basal rate. Frequency.

Distribution of the percentage differences of each basal rate estimate to final basal insulin rates. Distribution of the percentage differences of each.

Patient flow chart: the final prospective study population consisted of 521 individuals, 113 on basal insulin and 408 on OADs. *Plausibility: height (130–230 cm),

Three-dimensional summary images of results from shape analysis of hippocampus, caudate, putamen and globus pallidus from superior and inferior views,

Mean daily glucose concentration and frequency of hypoglycemia in long-term care residents with type 2 diabetes. Mean daily glucose concentration and frequency.

(A) Correlation between change in HbA1c and change in weight from baseline to week 24 in the liraglutide group. (A) Correlation between change in HbA1c.

Adjusted OR and SE for BMI≥30 kg/m2, BMI 25–29. 9 kg/m2, HbA1c≥6

Deletion of neuronal insulin receptor signaling reduces TG secretion, while the targeted knockout of insulin receptors restricted to the periphery increases.

A: PPG increment at week 26 for mealtime faster aspart versus IAsp.

A: Relative risk of experiencing one or more hypoglycemic events per participant at any time (24 h) and during the night (0000–0559 h) for Gla-300 vs.

Glucose, insulin, and AGE levels during an OGC before and after RT

Exogenous CRP administration causes fasting hyperglycemia and hyperinsulinemia without altering body composition. Exogenous CRP administration causes fasting.

Chronic brain insulin infusion reduces liver TG content independent of changes in body weight and food intake. Chronic brain insulin infusion reduces liver.

Prevalence of high SAT or high VAT by BMI category in women (A) and men (B) and by waist circumference category in women (C) and men (D). Prevalence of.

Left columns: Plasma glucose and serum insulin concentrations, circulating TF-PCA, and FVIIa activity before and during 24 h of selective hyperglycemia.

Mean ± SEM concentration of insulin in plasma and CSF and glucose in plasma 30 min after the intraperitoneal administration of DET or NPH insulin at different.

Current insulin dose (units/kg/day) during the DCCT/EDIC study by sex (black line for females) (A), DCCT intensive vs. conventional treatment group (black.

Measurement of insulin release from islets evoked by glucose, diazoxide, and high K+. Measurement of insulin release from islets evoked by glucose, diazoxide,

Insulin sensitivity in athletes and sedentary normal-weight and obese, young, and old individuals. Insulin sensitivity in athletes and sedentary normal-weight.

Glucose control performance (by CGM) characterized by median and interquartile range cumulative % time in glucose range (A), overall glucose (B), and insulin.

Intracerebroventricular (ICV) insulin infusion increases TG secretion.

Diabetes development in B6.H-2g7/RIP-B7.1 and control mice.

Glucose stimulates GLP-1 secretion from the perfused rat intestine by a dose- and absorption-dependent manner. Glucose stimulates GLP-1 secretion from.

Mean (±SE) plasma glucose concentrations before, during, and after infusions of octreotide (with growth hormone) with saline (•), with insulin replacement.

Proportion of patients experiencing documented symptomatic hypoglycemia (blood glucose

Metabolic parameters in the three groups of patients during l-arginine infusion. Metabolic parameters in the three groups of patients during l-arginine.

Effect of empagliflozin on efficacy parameters at week 18.

Kaplan-Meier survival analysis for all-cause and CVD mortality in 2,823 type 2 diabetic patients stratified by CKD according to each creatinine-based equation.

Changes in glycated hemoglobin (HbA1c) levels after 12 weeks’ treatment with lixisenatide (according to dose increase regimen) or placebo. Changes in glycated.

Glycemic control and body weight over 52 weeks.

Effects of vinegar (□) and placebo (⧫) on plasma glucose (A–C) and insulin (D–F) responses after a standard meal in control subjects, insulin-resistant.

Changes (means±posterior SDs) in HbA1c (A), fasting glucose (B), and body weight (C) by treatment condition based on missing not at random (MNAR) analyses.

Median (interquartile range) of sensor glucose (A) and insulin delivery (B) during closed-loop (solid red line and red shaded area) and control period.

Mean (± SE) plasma glucose concentrations, symptom scores, plasma epinephrine and glucagon concentrations, and relative rCBF (as measured by PET counts)

Time course of HbA1c (A), FPG (B), body weight (C), SMPG (D), and lipase (E) from week 0 to week 26. Time course of HbA1c (A), FPG (B), body weight (C),

The hyperbolic relationship between fasting insulin and Si (A) and AIRg and Si (B) for NFG (FPG

Clinical responses to therapy from baseline to week 24 and end point with last observation carried forward (LOCF). Clinical responses to therapy from baseline.

Mean changes (standard error) from baseline in A1C (A and B) and body weight (C and D) for patients with type 1 (A and C) or type 2 (B and D) diabetes.

Adjusted OR and SE for BMI≥30 kg/m2, BMI 25–29. 9 kg/m2, HbA1c≥6

Distribution of daily frequency of BGM

Doses of trial medication in the liraglutide groups (A) and in the placebo groups (B). Doses of trial medication in the liraglutide groups (A) and in the.

Postoperative blood glucose levels and total insulin requirement.

The solid line represents the point estimate of the treatment ORs at various levels along the x-axis that ranges from the minimum to the maximum observed.

Time course of daily basal and mealtime insulin dose (A), glycated hemoglobin (B), laboratory-measured clinic FPG (C), prebreakfast SMPG (D), SMPG profiles.

Change in first-phase insulin response (A) and pancreas triglyceride content (B) in responders and nonresponders at baseline (hatched bars), after VLCD.

Cumulative distributions of A1C and fasting plasma glucose values for the U.S. population aged ≥12 years without diabetes for each survey cycle: 1999–2000,

Four–time point diurnal profiles of plasma glucose concentrations (A) and AUCs (B) over quintiles of HbA1c. ○, AUC1; •, AUC2; ▴, AUC2 − AUC1 (differences.

Changes of major clinical and biochemical characteristics at baseline and during follow-up in different groups. Changes of major clinical and biochemical.

Cumulative mean numbers of confirmed (plasma glucose ≤3

Sensitivity and specificity of HbA1c, FPG, and 2hPG in identifying persons who developed diabetes within 10 years of screening among children and adolescents.

ERRs (degludec/glargine U100) of hypoglycemia in Hispanic and non-Hispanic patients during the SWITCH 2 trial. ERRs (degludec/glargine U100) of hypoglycemia.

Presentation transcript:

Results for HbA1c (A), severe or BG-confirmed symptomatic hypoglycemia (B), change in body weight (C), daily total insulin dose (D), FPG (E), and nine-point SMPG profiles (F). Results for HbA1c (A), severe or BG-confirmed symptomatic hypoglycemia (B), change in body weight (C), daily total insulin dose (D), FPG (E), and nine-point SMPG profiles (F). A: Mean observed values with error bars (SEM) based on FAS. B: Mean cumulative frequency based on the SAS. Severe or BG-confirmed symptomatic describes an episode that is severe according to the ADA classification or BG-confirmed by a plasma glucose value <3.1 mmol/L (<56 mg/dL) with symptoms consistent with hypoglycemia. C: Least square mean (LSMean) values with error bars (SE of estimated LSMean) based on FAS, using MMRM. D: Mean observed values with error bars (SEM) based on the SAS. E: Mean observed values with error bars (SEM) based on FAS. F: Mean observed values with error bars (SEM) based on FAS. *Statistically significant difference between EOT means in favor of IGlar U100 + IAsp vs. IDegLira. Liana K. Billings et al. Dia Care 2018;41:1009-1016 ©2018 by American Diabetes Association