In-depth mouse metabolic phenotyping revealed that obesity increased first-pass degradation of an incretin hormone GLP-1 with increased liver DPP4 expression and decreased sinusoidal blood flow rate, reducing active GLP-1 levels in peripheral circulation.
The aim of this pilot study was to determine the effect of a single dose of a novel delayed-release nutrient (DRN) on glucose, GLP-1, c-peptide, insulin, and appetite in adults with obesity and type 2 diabetes.
GLP-1-based therapies are critical for a patient-centered approach in choosing appropriate pharmacotherapy for T2DM and obesity while also taking into consideration comorbidities, such as cardiovascular and chronic kidney diseases.
In general, patients using GLP-1-RA were younger (mean [SD], 49.6 [10.8] years vs 59.3 [10.9] years), had lower mean (SD) glycosylated hemoglobin levels (8.5% [1.2%] vs 9.6 [1.7%]), had lower mean (SD) fasting plasma glucose levels (9.0 [1.9] mmol/L vs 10.8 [2.6] mmol/L), higher mean (SD) body mass indexes (29.4 [3.9] kg/m<sup>2</sup> vs 24.6 [3.1] kg/m<sup>2</sup>), had higher comorbidity of obesity (75% vs 15%), had a higher occurrence of hyperlipidemia (63% vs 44%), and had lower occurrence of neuropathy (13% vs 34%) when compared with those using insulin (P < 0.0001 for all).
Due to their overall safety and efficacy, glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are becoming one of the cornerstones for the management of both obesity and T2DM, and a novel alternative for the treatment of NAFLD.
This review discusses current and emerging therapeutic options with GLP-1 RAs and considers the next generation of novel peptide co-agonists with the potential for improved therapeutic outcomes in obesity and type 2 diabetes.
In this study, we evaluated metabolic properties of oral nutritional supplement epigallocatechin gallate (EGCG) in combination with GLP-1 agonist exendin-4 in a mouse model of dietary-induced diabetes and obesity.
We assessed the effect of the GLP-1 RA liraglutide 3.0 mg for 16 weeks in 14 obese individuals with pathogenic MC4R mutations (BMI 37.5 ± 6.8) and 28 matched control participants without MC4R mutation (BMI 36.8 ± 4.8).
(2017) report a proof-of-concept study using genetically engineered skin transplants that produce the incretin GLP-1 to prevent diet-induced obesity, suggesting a powerful approach for treating metabolic disorders.
These studies suggest that compound 4d behaves well in lowering body weight and maintaining energy expenditure without a chance of hyperglycaemia, 4d has strong clinical potential as an efficient GLP-1/GCGR agonist in the prevention and treatment of obesity and dyslipidemia.