Liraglutide High Sensitivity ELISA Kit

Obesity continues to pose a major public health risk to the United States and across the world, with an estimated one-third of adult Americans being defined as obese. Obesity treatment guidelines recommend the use of pharmacologic therapy in adults who have a body mass index (BMI) of 30 kg/m2 or higher or in patients with a BMI of 27 kg/m2 or higher who have at least one weight-related comorbid condition (e.g., hypertension, dyslipidemia, insulin resistance, type 2 diabetes mellitus). Liraglutide is a glucagon-like peptide-1 receptor agonist that has been successfully used in the treatment of type 2 diabetes for several years. Weight loss has been well described as an additional benefit with liraglutide therapy, which prompted the manufacturer to evaluate and develop a higher dose formulation specifically for the treatment of obesity. Liraglutide 3 mg/day was approved by the U.S. Food and Drug Administration for this indication in December 2014. We performed a search of the Medline database to identify relevant literature focused on liraglutide's role specifically in treating obesity. Five clinical trials with this primary end point were identified. Data demonstrated that liraglutide can successfully achieve weight-loss benchmarks of 5% or more and 10% or more loss from baseline. The most common adverse effects were gastrointestinal and mild to moderate in intensity. The cost of therapy is high, averaging over $1000/month for out-of-pocket expenses if insurance coverage is not available. Liraglutide is also available for delivery only by subcutaneous injection, which may represent a barrier for patients. Liraglutide 3 mg/day represents another pharmacologic option for the treatment of obesity.

Aims: To review the differences between the human glucagon-like peptide-1 (GLP-1) molecule and the analogue liraglutide, and to summarise key data from the liraglutide preclinical study programme showing the therapeutic promise of this new agent.
Key findings: Liraglutide is a full agonist of the GLP-1 receptor and shares 97% of its amino acid sequence identity with human GLP-1. Unlike human GLP-1, however, liraglutide binds reversibly to serum albumin, and thus has increased resistance to enzymatic degradation and a longer half-life. In preclinical studies, liraglutide demonstrated good glycaemic control, mediated by the glucose-dependent stimulation of insulin and suppression of glucagon secretion and by delayed gastric emptying. Liraglutide also had positive effects on body weight, beta-cell preservation and mass, and cardiac function.
Conclusions: The therapeutic promise of liraglutide is evident from preclinical data. Liraglutide showed the potential to provide good glycaemic control without increasing the risk of hypoglycaemia and, as with exenatide, but not dipeptidyl peptidase-4 inhibitors, to mediate weight loss. Although these benefits have subsequently been studied clinically, beta-cell mass can be directly studied only in animal models. In common with other incretin-based therapies, liraglutide showed the potential to modulate the progressive loss of beta-cell function that drives the continuing deterioration in glycaemic control in patients with type 2 diabetes. Body weight was lowered by a mechanism involving mainly lowered energy intake, but also potentially altered food preference and maintained energy expenditure despite weight loss.