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),

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Fig. 2. Change in (A) glycosylated hemoglobin (HbA1c) and (B) fasting plasma glucose (FPG). Group A: oral hypoglycemic agents (OHAs; sulfonylurea+metformin.

with undiagnosed diabetes mellitus by three diagnostic criteria

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

The prevalence of diabetes (A), impaired glucose tolerance (B), impaired fasting glucose (C), and impaired glucose metabolism (D) among those with Finnish.

Athena Philis-Tsimikas, MD The American Journal of Medicine

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

Average patient profile in terms of (A) previous therapy drug class and (B) complexity of previous regimen. Average patient profile in terms of (A) previous.

Differences in the glycated hemoglobin (HbA1c) levels.

(A) Fasting serum glucose (mg/dL), (B) fasting serum insulin (μU/mL), (C) plasma glycated albumin (GA; %) and (D) plasma fructosamine (μmol/L) measured.

Flowchart of literature search for the effect of fructose on glycemic end points (fasting glucose, fasting insulin, and glycated blood proteins [HbA1c.

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

The excess effect of 3 or 6 months low to moderate carbohydrate diet compared with high-carbohydrate diet on HbA1c (%) versus reported intake (Energy %)

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

Illustration of the causal inference scheme.

Glycated hemoglobin (HbA1c) trajectories among children during the first 5 years after diagnosis of type 1 diabetes, stratified by diagnostic era and diagnostic.

Change in random blood glucose level, body weight, and intraperitoneal glucose tolerance test (IPGTT) in streptozotocin (STZ)-induced diabetic mice. Change.

Screening, enrollment, and randomization of study participants (BMI, body mass index; CTG, conventional therapy group; HbA1c, glycated hemoglobin; HDL-C,

Correlation of E/e’ with age (A), gender (B), fasting insulin (C), and sulfonylurea use (SU) (D) among patients with type 2 diabetes mellitus. Correlation.

Fasting plasma adiponectin concentration in relation to body mass index (BMI) (A), waist circumference (B), acute insulin response (AIR) (C) and insulin.

Respondents’ perceptions on (A) the potential of IDegLira compared with basal-bolus therapy to improve patient motivation to reach their target blood glucose.

Gender differences in diabetes prevalence in 2009 in the general Portuguese population patients and in patients with CAP. Diabetes prevalence is higher.

Flow sheet over the primary study population as well as comparative individuals of “pre-diabetic” individuals followed from HUNT2 to HUNT3 (GAD, glutamic.

Estimated HR as a function of absolute change in glycated hemoglobin (HbA1c; from index to measurement 22–26 months after). Estimated HR as a function.

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

Changes in weight and body mass index (BMI) associated with quality improvement. Changes in weight and body mass index (BMI) associated with quality improvement.

Change in HbA1c and weight compared with baseline variables for the liraglutide group and the placebo group. Change in HbA1c and weight compared with baseline.

(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.

Kaplan-Meier plot of incident CVD according to the treatment group over a 4-year period following intensification of diabetes therapy. Kaplan-Meier plot.

Receiver operating characteristic analyses showing area under the curves with reference to 2-hour OGTT (A,B) and fasting plasma glucose (C,D). HbA1c, glycated.

Scatterplot showing the association between baseline weight and weight change at 1 year, relative to baseline for each treatment group. Scatterplot showing.

Scatterplot showing the association between change in HbA1c at 1 year and weight change at 1 year, relative to baseline for each treatment group. Scatterplot.

Adjusted annual percentage of quality indicators by prescription

(A) Rate of achieving targets for glycated hemoglobin (HbA1c), blood pressure (BP), and lipids in all subjects and (B) prevalence of nephropathy, retinopathy,

Schematic of screening program for diabetes mellitus (DM) during acute myocardial infarction (AMI). Schematic of screening program for diabetes mellitus.

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

Inclusion process. Inclusion process. Of 5200 eligible patients, 204 declined participation, 111 had diabetes >400 days before All New Diabetics in Scania.

Correlation between plasma C reactive protein (CRP) and angiopoietin-like protein 4 (ANGPTL4). Correlation between plasma C reactive protein (CRP) and.

Change in %A1C over 5 years in response to 12-week intensive lifestyle intervention used in a real-world clinical practice. Change in %A1C over 5 years.

Mean and interquartile glucose values for (A) random blood glucose, (B) fastingplasma glucose, (C) HbA1c, (D) 1-hour OGTT, (E) 2-hour OGTT and (F)triglycerides.

Comparison of receiver operating characteristic (ROC) curves for predicting oral glucose tolerance test (OGTT) 1 h postload glucose ≥155 mg/dL in (A) patients.

Estimated HR as a function of mean residual of glycated hemoglobin (HbA1c) measurements to the line connecting index HbA1c and HbA1c measurement 22–26 months.

Association between antibiotic purchases and glycated hemoglobin (HbA1c) values in patients with and without diabetic nephropathy. Association between.

Enrollment of patients.

Comparison of triglycerides AUC 480’ between IGT+reduced FPIS group, IGT+preserved FPIS group, and IGT+reduced FPIS+reduced FPIS and FPIS restitution with.

The correlation between visceral fat area (VFA) and body mass index (BMI) in patients with type 2 diabetes. The correlation between visceral fat area (VFA)

Fig. 3. (A) Least-squares (LS) mean difference in glycosylated hemoglobin (HbA1c) from baseline, and (B) LS mean difference in HbA1c from baseline over.

Mean (95% CI) fasting s-glucose at baseline and 6-month, 12-month, and 24-month follow-up, overall and by sex (A), and by baseline age (B), education (C),

Change in markers of glycometabolism and cardiovascular risk profile.

Interaction of updated mean serial HbA1c and serum triglyceride levels with sensory peripheral neuropathy over 7 years in 151 type 2 diabetic participants.

Mean decline in grip strength with aging by baseline quartile of fasting plasma glucose (FPG). Mean decline in grip strength with aging by baseline quartile.

Participant flow diagram for the ‘GNHIES98—longitudinal sample’ and the ‘DEGS1—cross-sectional sample’. Participant flow diagram for the ‘GNHIES98—longitudinal.

Associations of body mass index (BMI) levels with achieving targets for glycated hemoglobin (HbA1c), blood pressure (BP), and lipids in the upper panels.

Continuous associations

Mean decline in grip strength with aging is shown for participants categorized by baseline quartile of 2 h glucose (2HG). Mean decline in grip strength.

Percentage of weight loss over 5 years in response to 12-week intensive lifestyle intervention in a real-world clinical practice. Percentage of weight.

Oral glucose tolerance testing during hospitalization and at 4 months after infarction. Oral glucose tolerance testing during hospitalization and at 4 months.

(A) Oral glucose tolerance test (OGTT) glucose and (C) natural logarithm of insulin responses over time with SEM bars comparing the first tertile to the.

Proportion of patients experiencing documented symptomatic hypoglycemia (blood glucose

Relationship between week 24 A1C and week 24 BeAM in the exploratory analysis (A), the main analysis (only patients with A1C >7.0% at week 24 were included.

Glycemic control and body weight over 52 weeks.

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.

Number of events, the crude incidence rate, and the crude and adjusted HR with 95% CI for the association between pioglitazone use and all-cause mortality.

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.

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

Plasma glucose (A), serum insulin (B), serum C peptide (C) and plasma GLP-1 level (D) during the 2-hour OGTT among subjects with normal glucose tolerance.

Postprandial glucose, insulin and glucagon-like peptide-1 (GLP-1) levels following carbohydrate-first (CF), carbohydrate-last (CL) and sandwich (S) meal.

Patient disposition and study protocol.

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

Presentation transcript:

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), weight (40–200 kg), HbA1c (4–15%), FPG (2.8–13.9 mmol/L), PPG (≥3 mmol/L). 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), weight (40–200 kg), HbA1c (4–15%), FPG (2.8–13.9 mmol/L), PPG (≥3 mmol/L). DIVE, Diabetes Versorgungs-Evaluation; FPG, fasting plasma glucose; HbA1c, glycated hemoglobin; OAD, oral antidiabetic drug; PPG, postprandial glucose. Peter Bramlage et al. BMJ Open Diab Res Care 2017;5:e000301 ©2017 by American Diabetes Association