What is the action mechanism of Glucagon-like peptide-1 (GLP-1) agonists?

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From the Guidelines

GLP-1 agonists work by mimicking the action of the naturally occurring hormone glucagon-like peptide-1 (GLP-1), binding to GLP-1 receptors primarily in the pancreas, stimulating insulin secretion from beta cells in a glucose-dependent manner while simultaneously suppressing glucagon release from alpha cells, as reported in a recent narrative review 1.

Mechanism of Action

The mechanism of action of GLP-1 agonists involves several key steps:

  • Stimulating insulin secretion from beta cells in a glucose-dependent manner
  • Suppressing glucagon release from alpha cells
  • Slowing gastric emptying, which delays carbohydrate absorption and reduces post-meal blood glucose spikes
  • Acting on the brain's satiety center to decrease appetite and food intake, contributing to weight loss

Clinical Effects

The clinical effects of GLP-1 agonists include:

  • Lowering fasting plasma glucose and glycated haemoglobin in patients with type 2 diabetes mellitus 1
  • Promoting weight loss by delaying gastric emptying and increasing satiety, in patients with and without diabetes mellitus 1
  • Offering cardiovascular benefits and potentially having protective effects on the kidneys and liver, as shown in a meta-analysis 1

Common GLP-1 Agonists

Common GLP-1 agonists include:

  • Semaglutide (Ozempic, Wegovy, Rybelsus)
  • Liraglutide (Victoza, Saxenda)
  • Dulaglutide (Trulicity)
  • Exenatide (Byetta, Bydureon)
  • Tirzepatide (Mounjaro) These medications are typically administered as subcutaneous injections at varying frequencies (daily to weekly) depending on the specific agent, though oral semaglutide (Rybelsus) is taken daily by mouth 1.

From the FDA Drug Label

Semaglutide acts as a GLP-1 receptor agonist that selectively binds to and activates the GLP-1 receptor, the target for native GLP-1. Semaglutide reduces blood glucose through a mechanism where it stimulates insulin secretion and lowers glucagon secretion, both in a glucose-dependent manner. Liraglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase by the stimulatory G-protein, Gs, in pancreatic beta cells. Liraglutide increases intracellular cyclic AMP (cAMP) leading to insulin release in the presence of elevated glucose concentrations Liraglutide also decreases glucagon secretion in a glucose-dependent manner.

The GLP-1 agonists mechanism of action involves:

  • Stimulating insulin secretion in a glucose-dependent manner
  • Lowering glucagon secretion in a glucose-dependent manner
  • Delaying gastric emptying, reducing the rate at which glucose appears in the circulation postprandially The action mechanism of GLP-1 agonists, such as semaglutide and liraglutide, is to activate the GLP-1 receptor, leading to increased insulin secretion and decreased glucagon secretion, resulting in lowered blood glucose levels 2 3.

From the Research

GLP-1 Agonists Action Mechanism

The action mechanism of GLP-1 agonists involves several key aspects:

  • Augmentation of hyperglycemia-induced insulin secretion 4, 5, 6
  • Suppression of glucagon secretion at hyper- or euglycemia 4, 5, 6
  • Deceleration of gastric emptying, preventing large post-meal glycemic increments 4, 5, 6
  • Reduction in calorie intake and body weight 4, 5, 6

Differences Between Short-Acting and Long-Acting GLP-1 RAs

The primary pharmacodynamic difference between short-acting and long-acting GLP-1 RAs is:

  • Short-acting agents primarily delay gastric emptying, lowering postprandial glucose 5
  • Long-acting agents affect both fasting glucose and postprandial glucose, via enhanced glucose-dependent insulin secretion and reduced glucagon secretion in the fasting state 5

Therapeutic Implications

GLP-1 agonists have therapeutic implications for:

  • Treatment of type 2 diabetes 4, 5, 7
  • Obesity 8
  • Neurodegenerative disorders 6, 8
  • Cardiovascular disease 4, 6

Key Effects of GLP-1

The key effects of GLP-1 include:

  • Glucose-dependent stimulation of insulin secretion 6, 8
  • Decrease of gastric emptying 6, 8
  • Inhibition of food intake 6, 8
  • Modulation of rodent β-cell proliferation 8
  • Cardio- and neuroprotective effects 8

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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