scholarly journals Liraglutide in Combination with Metformin or Sulfonylurea for the Treatment of Type 2 Diabetes in Adult patients

2012 ◽  
Vol 4 ◽  
pp. CMT.S7283
Author(s):  
Maneesh V Udiawar ◽  
Stephen C Bain
Keyword(s):  
Type 2 Diabetes ◽  
Clinical Trials ◽  
Cell Function ◽  
Β Cell ◽  
Beneficial Effects ◽  
Number Of Patients ◽  
Β Cell Function ◽  
Glucagon Like Peptide 1 ◽  
Glycemic Targets

Type 2 diabetes is a progressive disease characterized by decline in β-cell function and insulin resistance. The development of liraglutide, a glucagon-like peptide 1 (GLP-1) receptor agonist, has been shown in clinical trials to be an effective drug with beneficial effects on β-cell function and improved glycemic control, without the side effects of weight gain and hypoglycemia that frequently limit the use of oral anti-diabetic drugs. Furthermore, its prolonged half-life makes it suitable for once daily administration. Liraglutide is demonstrated to be an effective agent in combination with commonly used oral antidiabetic drugs such as metformin and sulphonylureas, with a significant number of patients achieving their glycemic targets without hypoglycemia. In this review, the results from clinical trials utilizing liraglutide in combination with metformin or sulphonylurea are summarized with regards to efficacy and safety.

scholarly journals Exploiting the antidiabetic properties of incretins to treat type 2 diabetes mellitus: glucagon-like peptide 1 receptor agonists or insulin for patients with inadequate glycemic control?

2008 ◽  
Vol 158 (6) ◽  
pp. 773-784 ◽  
Author(s):  
Luc F Van Gaal ◽  
Stephen W Gutkin ◽  
Michael A Nauck
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Body Weight ◽  
Cell Function ◽  
Β Cell ◽  
Β Cell Function ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Type 2 diabetes mellitus is associated with progressive decreases in pancreatic β-cell function. Most patients thus require increasingly intensive treatment, including oral combination therapies followed by insulin. Fear of hypoglycemia is a potential barrier to treatment adherence and glycemic control, while weight gain can exacerbate hyperglycemia or insulin resistance. Administration of insulin can roughly mimic physiologic insulin secretion but does not address underlying pathophysiology. Glucagon-like peptide 1 (GLP-1) is an incretin hormone released by the gut in response to meal intake that helps to maintain glucose homeostasis through coordinated effects on islet α- and β-cells, inhibiting glucagon output, and stimulating insulin secretion in a glucose-dependent manner. Biological effects of GLP-1 include slowing gastric emptying and decreasing appetite. Incretin mimetics (GLP-1 receptor agonists with more suitable pharmacokinetic properties versus GLP-1) significantly lower hemoglobin A1c, body weight, and postprandial glucose excursions in humans and significantly improve β-cell function in vivo (animal data). These novel incretin-based therapies offer the potential to reduce body weight or prevent weight gain, although the durability of these effects and their potential long-term benefits need to be studied further. This article reviews recent clinical trials comparing therapy with the incretin mimetic exenatide to insulin in patients with oral treatment failure, identifies factors consistent with the use of each treatment, and delineates areas for future research.

scholarly journals Exaggerated Glucagon-Like Peptide 1 Response Is Important for Improved β-Cell Function and Glucose Tolerance After Roux-en-Y Gastric Bypass in Patients With Type 2 Diabetes

Diabetes ◽  
2013 ◽  
Vol 62 (9) ◽  
pp. 3044-3052 ◽  
Author(s):  
Nils B. Jørgensen ◽  
Carsten Dirksen ◽  
Kirstine N. Bojsen-Møller ◽  
Siv H. Jacobsen ◽  
Dorte Worm ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Gastric Bypass ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Β Cell ◽  
Β Cell Function ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Pathogenetic substantiation and effectiveness of vildagliptin use inpatients with diabetes mellitus type 2

2009 ◽  
Vol 6 (3) ◽  
pp. 16-26 ◽  
Author(s):  
T I Romantsova
Keyword(s):  
Type 2 Diabetes ◽  
Cell Function ◽  
Glucagon Secretion ◽  
Β Cell ◽  
Dipeptidyl Peptidase 4 ◽  
Glucose Levels ◽  
Β Cell Function ◽  
Control Of Diabetes ◽  
Glucagon Like Peptide 1

Insulin resistance in muscle and liver and β-cell failure represent the core pathophysiologic defects in type 2 diabetes. Now it isrecognized that the β-cell failure occurs much earlier and is more severe than previously thought. As a result, earlier and more aggressive new therapy is needed to achiev e better control of diabetes and to prev ent/slow the progressive B-cell failure that already is w ell established in IGT subjects. One approach is to target the incretin mimetic hormone glucagon-like peptide-1 (GLP-1). When blood glucose levels are elevated, GrP-1 stimulates insulin secretion, decreases glucagon secretion, impro ves β-cell function, and slows gastric emptying. GrP-1 production is reduced in patients with type 2 diabetes. Furthermore, GrP-1 is rapidly degraded by the dipeptidyl peptidase 4 (DPP-4) enzyme. Trials have showed, that new inhibitor DPP-4 vildagliptin (Galvus) hav e been demonstrated to significantly reduce HbA lc, fasting and prandial glucose levels when used as monotherapy and in соmbination with traditional agents. Advantages of vildagliptin include few adverse events, low risk of hypoglycemia, neutral effect on body weight, and a once-daily oral dosing regimen. Inaddition, vildagliptin may preserve the decline in β-cell function. Hence, vildagliptin may modify the natural progressive course of diabetes; this however, must be confirmed with longer-term controlled studies

scholarly journals Irisin and Incretin Hormones: Similarities, Differences, and Implications in Type 2 Diabetes and Obesity

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 286
Author(s):  
Nicola Marrano ◽  
Giuseppina Biondi ◽  
Anna Borrelli ◽  
Angelo Cignarelli ◽  
Sebastio Perrini ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Weight Loss ◽  
Energy Homeostasis ◽  
Cell Function ◽  
Gut Hormones ◽  
Insulin Biosynthesis ◽  
Β Cell ◽  
Beneficial Effects ◽  
Β Cell Function

Incretins are gut hormones that potentiate glucose-stimulated insulin secretion (GSIS) after meals. Glucagon-like peptide-1 (GLP-1) is the most investigated incretin hormone, synthesized mainly by L cells in the lower gut tract. GLP-1 promotes β-cell function and survival and exerts beneficial effects in different organs and tissues. Irisin, a myokine released in response to a high-fat diet and exercise, enhances GSIS. Similar to GLP-1, irisin augments insulin biosynthesis and promotes accrual of β-cell functional mass. In addition, irisin and GLP-1 share comparable pleiotropic effects and activate similar intracellular pathways. The insulinotropic and extra-pancreatic effects of GLP-1 are reduced in type 2 diabetes (T2D) patients but preserved at pharmacological doses. GLP-1 receptor agonists (GLP-1RAs) are therefore among the most widely used antidiabetes drugs, also considered for their cardiovascular benefits and ability to promote weight loss. Irisin levels are lower in T2D patients, and in diabetic and/or obese animal models irisin administration improves glycemic control and promotes weight loss. Interestingly, recent evidence suggests that both GLP-1 and irisin are also synthesized within the pancreatic islets, in α- and β-cells, respectively. This review aims to describe the similarities between GLP-1 and irisin and to propose a new potential axis–involving the gut, muscle, and endocrine pancreas that controls energy homeostasis.

Liraglutide – A Once-daily Human Glucagon-like Peptide-1 Analogue Treatment for Type 2 Diabetes

2009 ◽  
Vol 05 (0) ◽  
pp. 38
Author(s):  
Chantal Mathieu ◽  
Keyword(s):  
Type 2 Diabetes ◽  
Cell Function ◽  
Patient Acceptance ◽  
Β Cell ◽  
Dipeptidyl Peptidase 4 ◽  
Receptor Agonists ◽  
Β Cell Function ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Type 2 diabetes is a progressive disease characterised by deteriorating β-cell function and glycaemic control. To counter this, affected individuals require regular intensification of their antidiabetes treatments to provide appropriate metabolic control. However, current treatment options – such as sulphonylureas, thiazolidinediones and insulins – induce weight gain, which can reduce patient acceptance and/or compliance with treatment and may have significant health implications. In addition, many of the antidiabetic therapies raise the risk of hypoglycaemic episodes. Therefore, patients, physicians and healthcare providers are looking for new therapeutic options to address this large and growing burden of diabetes. Incretin-based therapies – including glucagon-like peptide-1 (GLP-1) receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors – are becoming a popular treatment option for patients with type 2 diabetes because they offer many benefits compared with other antidiabetic therapies. First, incretin-based therapies are associated with significant reductions in glycated haemoglobin (HbA1c) with a low inherent risk of hypoglycaemic events. In addition, GLP-1 receptor agonists are associated with reductions in bodyweight and systolic blood pressure. Incretin-based therapies such as liraglutide also offer the potential to improve β-cell function, an important underlying mechanism of type 2 diabetes.

Nutrient regulation of pancreatic β-cell function in diabetes: problems and potential solutions

2006 ◽  
Vol 34 (5) ◽  
pp. 774-778 ◽  
Author(s):  
P.R. Flatt ◽  
B.D. Green
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Cell Function ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Intestinal Hormones ◽  
Nutrient Regulation ◽  
Β Cell Function ◽  
Glucagon Like Peptide 1

Increasing prevalence of obesity combined with longevity will produce an epidemic of Type 2 (non-insulin-dependent) diabetes in the next 20 years. This disease is associated with defects in insulin secretion, specifically abnormalities of insulin secretory kinetics and pancreatic β-cell glucose responsiveness. Mechanisms underlying β-cell dysfunction include glucose toxicity, lipotoxicity and β-cell hyperactivity. Defects at various sites in β-cell signal transduction pathways contribute, but no single lesion can account for the common form of Type 2 diabetes. Recent studies highlight diverse β-cell actions of GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide). These intestinal hormones target the β-cell to stimulate glucose-dependent insulin secretion through activation of protein kinase A and associated pathways. Both increase gene expression and proinsulin biosynthesis, protect against apoptosis and stimulate replication/neogenesis of β-cells. Incretin hormones therefore represent an exciting future multi-action solution to correct β-cell defect in Type 2 diabetes.

Sign in / Sign up

Export Citation Format

Share Document