Glucagon-like peptide-1 receptor agonists (GLP-1 RA) are now routinely used in the management of type 2 diabetes due to their additional benefits beyond glycemic control. However, there is limited data on their efficacy in real clinical practice, and the purpose of this study is to compare the clinical efficacy of GLP-1 RAs by comparing A1c lowering and weight reduction between these agents.
Glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium–glucose cotransporter 2 inhibitors (SGLT2is) are widely used to treat type 2 diabetes (T2D), but trial data on their combined use are limited. We report the first data on oral semaglutide in combination with SGLT2i. This was a posthoc subgroup analysis of the 52-week, double-blind, double-dummy PIONEER 4 trial (NCT02863419), in which patients with T2D uncontrolled on metformin with or without SGLT2i were randomized 2:2:1 to once-daily oral semaglutide 14 mg, subcutaneous (s.c.) liraglutide 1.8 mg or placebo.
In an exploratory analysis of 7 global phase 3a trials (PIONEER 1–5, 7 and 8), we evaluated the effect of age at baseline on efficacy (<45, ≥45 – <65 or ≥65 years) and safety (<65 or ≥65 years) for oral semaglutide (3, 7, 14 mg once daily) vs comparators in patients with type 2 diabetes. Efficacy endpoints: change from baseline in glycated hemoglobin (HbA1c) and body weight. Across all trials, there were 582, 3,392 and 1,683 patients aged <45, ≥45 – <65 and ≥65 years, respectively. Baseline HbA1c was similar across age groups, whereas baseline body weight tended to be higher in younger patients.
The global PIONEER program investigated the efficacy and safety of the first oral glucagon-like peptide-1 receptor agonist, oral semaglutide. Across PIONEER trials, patients with type 2 diabetes (T2D) were randomized to once-daily oral semaglutide (3, 7, 14 mg or flexibly dosed) or comparator. The present exploratory subgroup analysis evaluated the effect of background medications on glycated hemoglobin (HbA1c) and body weight (BW) reductions at the end of trial (week 26, 52 or 78) in 5 PIONEER trials (3–5, 7–8).
In the SUSTAIN trial program, once-weekly (OW) semaglutide, a GLP-1RA approved for type 2 diabetes treatment, significantly reduced HbA1c and body weight (BW) vs all comparators, with a safety profile consistent with the GLP-1RA class.
The global PIONEER program investigated the efficacy and safety of oral semaglutide, a glucagon-like peptide-1 receptor agonist. Patients with type 2 diabetes were randomized to once-daily oral semaglutide (3, 7 or 14 mg, or flexibly dosed [flex]), placebo or active comparator (empagliflozin 25 mg, sitagliptin 100 mg or liraglutide 1.8 mg). This exploratory subgroup analysis evaluated the effect of race on glycated hemoglobin (HbA1c) and body weight (BW) reductions at the end of treatment (week 26, 52 or 78).
In the phase 3 SUSTAIN clinical trial program, once-weekly semaglutide was more effective than comparators at lowering HbA1c and body weight in subjects with type 2 diabetes (T2D). This posthoc analysis of SUSTAIN 1–5 and 7–10 compared efficacy of semaglutide in subjects <65 years (nonelderly) with those ≥65 years (elderly) vs placebo and active comparators. These comparisons were reported individually, by trial.
This posthoc analysis assessed change in HbA1c and body weight with once-weekly (OW) semaglutide in the phase 3 SUSTAIN 1–5 and 7–10 trials by baseline HbA1c subgroup.
The PIONEER phase 3 program investigated glycemic response and other efficacy endpoints in patients with type 2 diabetes randomized to oral semaglutide (3, 7 or 14 mg once daily), placebo or active comparator (empagliflozin 25 mg, sitagliptin 100 mg or liraglutide 1.8 mg once-daily). This posthoc analysis of PIONEER 1–5 and 8 trials evaluated the response of any reduction in HbA1c (%) and/or body weight (%), and a clinically relevant composite endpoint of HbA1c reduction ≥1% and body weight loss ≥5% with semaglutide 14 mg vs comparators at treatment end (26–78 weeks).
In the SUSTAIN clinical trials, once-weekly (OW) subcutaneous semaglutide demonstrated superior glycated hemoglobin (HbA1c) and body weight (BW) reductions in adults with type 2 diabetes (T2D). SURE Canada (NCT03457012) is a multicentre, prospective, noninterventional study investigating the effectiveness of OW semaglutide in a real-world setting.
To compare initiation of a fixed-ratio combination of glargine-lixisenatide (iGlarLixi) and insulin glargine U100 (iGlar), exclusively in South Asian origin Canadians.
In tandem with dyslipidemia, approximately 70% of patients with type 2 diabetes will develop nonalcoholic fatty liver disease, a chronic disease that ranges from simple steatosis to severe cirrhosis characterized by inflammation and fibrosis. Previous studies have demonstrated that circulating DPP4 is shed from hepatocytes and has a direct proinflammatory role in liver and adipose tissue. Therefore, this study aimed to evaluate the efficacy of eliminating hepatic Dpp4 in the progression of liver disease.
Sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1RA) have shown benefits in patients with diabetes and cardiovascular disease (CVD), and increasing evidence indicates benefits in those with chronic kidney disease (CKD) and heart failure. This study aims to describe current glucose-lowering medication prescribing patterns in Northern Alberta primary care settings.
Hypertension in type 2 diabetes patients (T2DP) contributes significantly to myocardial infarction and stroke. Unknown is the impact of flaxseed lignan complex (FLC) on Diabetes Canada’s clinical practice guidelines-defined (DCCPG-D) systolic hypertension (SH) and/or diastolic hypertension (DH) in older T2DP. It was hypothesized that FLC (600 mg secoisolariciresinol diglucoside (SDG)/day) for 3 months would decrease DCCPG-D SH and/or DH in older T2DP. The objective was to test this hypothesis.
Increased evidence on the real-world age- and sex-specific incidence of severe hypoglycemia (SH) in type 2 diabetes (T2DM) could reveal straightforward yet impactful targets for improved clinical and public health interventions.
Youth-onset type 2 diabetes (T2D) is increasing worldwide. The prevalence of dysglycemia and microalbuminuria prior to diagnosis remains unclear. This project examined the presence of dysglycemia and albuminuria prior to diagnosis in youth with T2D, and compared rates of albuminuria in youth-onset T2D compared to normoglycemic youth.
Insulin dysregulation independently underlies diabetes and Alzheimer’s Disease (AD). The former has also been shown to be a risk factor for the latter. The ancestral insulin gene (Ins2), but not the Ins1 gene, is transcribed locally within the brain in mice. We confirmed that neuronal expression of Ins2 is abundant within the hippocampus, a region with established roles in learning and memory. Public single cell RNA sequencing datasets were analyzed to determine the specific cell types where Ins2 is expressed in the mouse brain.
Epidemiological studies have shown hyperinsulinemia is independently associated with increased pancreatic ductal adenocarcinoma (PDAC) morbidity and mortality. We recently showed direct in vivo evidence that hyperinsulinemia promotes PDAC. Using a mouse model of PDAC development (Ptf1aCreER;LSL-KrasG12D) crossed with Ins1+/-;Ins2-/- alleles that result in ∼50% reduced fasting insulin, we found a ∼50% reduction in pancreatic intraepithelial neoplasia (PanIN) precancerous lesions compared with Ins1+/+;Ins2-/- control mice.
Development and thorough characterization of genetic tools is necessary for efficient and productive understanding of the beta cell. Over the past few years, multiple mouse lines expressing Cre recombinase in beta cells have been developed, but all have significant caveats towards their use. Our laboratory has invested significant effort into characterizing new and existing lines to provide a model for the beta cell community. Our goal is to provide a mouse that 1) has efficient, inducible Cre expression; 2) only in beta cells and 3) limits the need for drug administration (i.e.
In individuals living with obesity without diabetes, β-cell mass accretion maintains glucose homeostasis by balancing levels of circulating insulin and insulin resistance. Type 2 diabetes appears when these compensatory mechanisms fail. Deciphering the pathways controlling β-cell proliferation has, thus, become a major research goal in the hope to identify therapeutic targets to expand β-cell mass and prevent or delay the onset of diabetes. Previously, we demonstrated that the fatty acid mixture ClinOleic (65% oleate) potentiates glucose-induced β-cell proliferation in vivo in rats.
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