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GLP-1 receptor agonists differ substantially in their duration of action, frequency of administration and clinical profile. This article reviews the mechanisms of action and clinical evidence for GLP-1 receptor targeting and discusses differences between GLP-1 therapies, focusing particularly on clinical data for the GLP-1 receptor agonist, lixisenatide. Different GLP-1 therapies exert differential effects on fasting and postprandial glycemia both being major determinants of glycemic control. They also slow gastric emptying to different extents, probably accounting for different effects to reduce postprandial glycemia. The GetGoal phase 3 studies in T2DM have confirmed the efficacy of once-daily lixisenatide in reducing plasma glucose and glycated hemoglobin HbA 1c , with a pronounced lowering of postprandial plasma glucose PPG , as monotherapy and as add-on to oral antidiabetic drugs and to basal insulin. Lixisenatide is generally well tolerated, with possibly better gastrointestinal tolerability and lower risk of hypoglycemia than exenatide immediate release.
Post hoc analyses of fasting biomarkers and multiple linear regression analysis. Analyze biomarkers of beta-cell function and insulin resistance IR and evaluate WL contributions to IR improvements at 26 weeks. To determine whether improvements in IR were directly attributable to WL, multiple linear regression analysis with potential confounding variables age, sex, metformin, triglycerides, and glycated hemoglobin A1c was conducted. Tirzepatide improved markers of IS and beta-cell function to a greater extent than dulaglutide. IS effects of tirzepatide were only partly attributable to WL, suggesting dual receptor agonism confers distinct mechanisms of glycemic control.
Freeman JS. The Pathophysiologic Role of Incretins. Many patients with type 2 diabetes mellitus T2DM are unable to achieve adequate glycemic control. The incretin mimetics are a new class of medications available for treating patients with T2DM. They mimic the action of incretins, which are peptide hormones that originate in the gastrointestinal tract. These hormones are released during nutrient absorption, augmenting insulin secretion. The glycemic profiles of patients after administration of incretin mimetics and DPP-IV inhibitors show improvement in postprandial glucose levels and ultimately in HbA 1c.
Glucagon-like peptide-1 GLP-1 is a 30 or 31 amino acid long peptide hormone deriving from the tissue-specific posttranslational processing of the proglucagon peptide. It is produced and secreted by intestinal enteroendocrine L-cells and certain neurons within the nucleus of the solitary tract in the brainstem upon food consumption. The initial product GLP-1 1—37 is susceptible to amidation and proteolytic cleavage which gives rise to the two truncated and equipotent biologically active forms, GLP-1 7—36 amide and GLP-1 7— Alongside glucose-dependent insulinotropic peptide GIP , GLP-1 is an incretin ; thus, it has the ability to decrease blood sugar levels in a glucose-dependent manner by enhancing the secretion of insulin. Beside the insulinotropic effects, GLP-1 has been associated with numerous regulatory and protective effects.
Obesity is a major cause of cardiovascular disease and cancer, and its prevalence is increasing worldwide 1. Thus, it is critical to find effective treatments. An important issue is the regain of weight after different lifestyle interventions. This is at least partly due to resumption of previous lifestyle habits but also has physiological reasons.
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Glucose-dependent insulinotropic polypeptide GIP is a member of the incretin hormones and growth factors. Neurons express the GIP receptor, and GIP and its agonists can pass through the blood brain barrier and show remarkable neuroprotective effects by protecting synapse function and numbers, promoting neuronal proliferation, reducing amyloid plaques in the cortex and reducing the chronic inflammation response of the nervous system. Long-acting analogues of GIP that are protease resistant had been developed as a treatment for type 2 diabetes. Novel dual agonist peptides that activate the GIP receptor and another incretin receptor, glucagon-like peptide -1 GLP-1 , are under development that show superior effects in diabetic patients compared to single GLP-1 agonists. Therefore, the key triggers that induce the development of AD are most likely environmental, and it is very difficult to assess what these initial causes may be. Therefore, a promising approach to investigate what potential contributing factors there are is the correlation of AD onset with other factors that increase the risk of developing AD. Several such risk factors have been identified, and type 2 diabetes is one of these.
Mice were treated with multiple low dose streptozotocin or hydrocortisone. Islet parameters were assessed by immunohistochemistry and hormone measurements were determined by specific enzyme linked immunoassays. In contrast, hydrocortisone treatment and induction of insulin resistance increased islet numbers and area, with enhanced beta cell replication, elevated mass of beta and alpha cells, together with co-expression of GLP-1 and GIP with glucagon in islets. In contrast, both groups of mice lacking functional incretin receptors displayed substantially impaired islet adaptations to insulin resistance induced by hydrocortisone, including marked curtailment of expansion of islet area, beta cell mass and islet number. Our observations cannot be explained by simple changes in circulating incretin concentrations, suggesting that intra-islet GLP-1 and GIP make a significant contribution to islet adaptation, particularly expansion of beta cell mass and compensatory islet compensation to hydrocortisone and insulin resistance. This is an open-access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Data Availability: The authors confirm that all data underlying the findings are fully available without restriction.
GLP-1 is an incretin (hormone that increases insulin secretion in Site of Production GIP K-cells (Duodenum and Jejunum) GLP-1 L-cells (Ileum Available at: rithillel.org#page=1; 3.
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