scholarly journals The Relationship between Composite Measures of Glycemic Control and Beta-Cell Function in Type 2 Diabetes

2017 ◽  
Vol 4 (1) ◽  
Author(s):  
Klaus Dieter Kohnert
Keyword(s):  
Type 2 Diabetes ◽  
Glycemic Control ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Composite Measures ◽  
The Relationship

scholarly journals Effect of sitagliptin on glycemic control and beta cell function in Japanese patients given basal-supported oral therapy for type 2 diabetes

2014 ◽  
Vol 61 (12) ◽  
pp. 1213-1220 ◽  
Author(s):  
Shiko Asai ◽  
Akio Ohta ◽  
Hiroyuki Kato ◽  
Yoshiyuki Sada ◽  
Yoshio Nagai ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glycemic Control ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Oral Therapy ◽  
Cell Function ◽  
Japanese Patients ◽  
Basal Supported Oral Therapy

scholarly journals Association between beta cell function and future glycemic control in patients with type 2 diabetes

2012 ◽  
Author(s):  
Yoshifumi Saisho ◽  
Kinsei Kou ◽  
Kumiko Tanaka ◽  
Takayuki Abe ◽  
Akira Shimada ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glycemic Control ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function

1270-P: Glycemic Control in Youth with Type 2 Diabetes Correlates with Weight Loss and Markers of Beta-Cell Function, but Not Intense Insulin Regimen

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1270-P
Author(s):  
LILY CHAO ◽  
MEIYU YEH ◽  
JENNIFER RAYMOND ◽  
JI HOON RYOO ◽  
NANCY T. CHANG
Keyword(s):  
Type 2 Diabetes ◽  
Weight Loss ◽  
Glycemic Control ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Insulin Regimen

scholarly journals Short-term insulin therapy at the time of diagnosis of Type 2 diabetes leads to better glycemic control and improved beta cell function

2019 ◽  
Vol 10 (3) ◽  
pp. 97 ◽  
Author(s):  
Viswanathan Mohan ◽  
Siddharth Madnani ◽  
RanjitMohan Anjana ◽  
SanjayBaliram Warade ◽  
Muthukrishnan Varalakshmi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glycemic Control ◽  
Beta Cell ◽  
Insulin Therapy ◽  
Beta Cell Function ◽  
Cell Function ◽  
Short Term

The Incretin System and Type 2 Diabetes

2009 ◽  
Vol 05 (01) ◽  
pp. 57 ◽  
Author(s):  
Anthony H Barnett ◽  
Keyword(s):  
Type 2 Diabetes ◽  
Glycemic Control ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Cell Mass ◽  
Pancreatic Islet Cell ◽  
Receptor Agonists

While antidiabetes therapies target glycemic control, most do not address the underlying problems of excess bodyweight and deteriorating pancreatic beta-cell function. Some therapies also provoke hypoglycemia and/or weight gain. Glucagon-like peptide-1 (GLP-1) is an incretin hormone secreted by the gut in response to nutrient intake and has a major role in the post-prandial insulin response in healthy individuals. The incretin response is, however, impaired in individuals with type 2 diabetes. There are two therapeutic approaches that target the incretin system: GLP-1 receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors. GLP-1 receptor agonists provide pharmacological levels of GLP-1 activity, while DPP-4 inhibitors restore physiological levels. The pharmacological levels of GLP-1 induced by GLP-1 receptor agonists provide effective glycemic control and weight reduction. The DPP-4 inhibitors also improve glycemic control but are weight-neutral. Pre-clinical studies in animal models andin vitrosystems suggest that incretin-based therapies have the potential to preserve beta-cell mass and improve their function. Initial clinical data show improvements in beta-cell function in patients treated with incretin-based therapies, supporting the pre-clinical observations. A further benefit of incretin-based therapies is that they provide glucose-dependent glucose control, which means that they have a low inherent risk of inducing hypoglycemia. These agents therefore look extremely promising in the management of type 2 diabetes, being efficacious and having positive benefits on weight, low risk of hypoglycemia, and the potential to improve pancreatic islet cell function in the long term.

78-OR: Glycaemia, Beta-Cell Function, and Incretin Hormones Post-OGTT One Year after Gastric Bypass and Sleeve Gastrectomy in Patients with Morbid Obesity and Type 2 Diabetes: An RCT (Oseberg Study)

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 78-OR
Author(s):  
FARHAT FATIMA ◽  
JØRAN HJELMESÆTH ◽  
KARE I. BIRKELAND ◽  
HANNE L. GULSETH ◽  
JENS K. HERTEL ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Morbid Obesity ◽  
Gastric Bypass ◽  
Sleeve Gastrectomy ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Incretin Hormones ◽  
One Year

scholarly journals Effects of efpeglenatide versus liraglutide on gastric emptying, glucose metabolism and beta-cell function in people with type 2 diabetes: an exploratory, randomized phase Ib study

2021 ◽  
Vol 9 (1) ◽  
pp. e002208
Author(s):  
Marcus Hompesch ◽  
Jahoon Kang ◽  
OakPil Han ◽  
Michael E Trautmann ◽  
Christopher H Sorli ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Gastric Emptying ◽  
Glucose Metabolism ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Phase Ib ◽  
Link Type ◽  
Drug Concentrations

IntroductionTo evaluate the effects of efpeglenatide, a long-acting glucagon-like peptide-1 receptor agonist (GLP-1 RA), on gastric emptying, glucose metabolism, and islet beta-cell function versus liraglutide and placebo in people with type 2 diabetes.Research design and methodsThis phase Ib study (ClinicalTrials.gov identifier: NCT02059564) randomized participants (n=47) to three cohorts. Within the first two cohorts, participants were randomized to placebo, efpeglenatide 6 mg weekly (QW; first cohort), or efpeglenatide 16 mg monthly (QM; second cohort). The third cohort received liraglutide 1.8 mg daily (QD). Gastric emptying was assessed through the pharmacokinetic (PK) profile of acetaminophen at baseline and steady state. Glucose metabolism and beta-cell function were assessed based on mixed-meal tolerance testing and a graded glucose infusion procedure.ResultsTreatment duration was approximately 3 months for efpeglenatide 16 mg QM and 1 month for efpeglenatide 6 mg QW and liraglutide. At peak drug concentrations, efpeglenatide 6 mg QW was non-inferior to liraglutide 1.8 mg QD in delaying gastric emptying, as assessed by acetaminophen PK (lower bound of 90% CI for the efpeglenatide:liraglutide ratio >0.8 for area under the curve (AUC)0–120, AUC0–180, AUC0–360 and maximum concentration (Cmax)). Efpeglenatide 16 mg QM did not decrease the rate of gastric emptying to as great an extent as liraglutide (ie, non-inferiority was not shown). Compared with liraglutide, both efpeglenatide dosing regimens demonstrated comparable or more favorable glucometabolic effects and improved beta-cell function. All gastrointestinal adverse events reported with efpeglenatide were mild or moderate in severity and transient over treatment and follow-up.ConclusionsThe glucometabolic effects of efpeglenatide 6 mg QW and 16 mg QM were comparable to liraglutide. Additional studies are necessary to further examine these benefits of efpeglenatide.Trial registration numberNCT02059564.

Insulin resistance and beta cell function in aboriginals with type 2 diabetes in Atlantic Canada

2000 ◽  
Vol 50 ◽  
pp. 108 ◽  
Author(s):  
Meng H. Tan ◽  
Sethu Reddy ◽  
Jean Abram ◽  
Pantelis Andreou ◽  
Danita Volder
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Atlantic Canada
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