GLP-1, GIP & Multi-Agonist Terms
Definitions related to incretin hormones, receptor agonists, and multi-receptor peptide pathways commonly referenced in metabolic and endocrine research.
- Incretin Hormone
- A class of metabolic hormones released after eating that stimulate insulin secretion and regulate glucose metabolism.
- GLP-1 (Glucagon-Like Peptide-1)
- An incretin hormone that enhances insulin secretion, suppresses glucagon release, and slows gastric emptying.
- GIP (Glucose-Dependent Insulinotropic Polypeptide)
- An incretin hormone that stimulates insulin release in response to nutrient intake.
- Glucagon
- A hormone that raises blood glucose levels by promoting glucose release from the liver.
- GLP-1 Receptor (GLP-1R)
- A receptor activated by GLP-1 that mediates insulin secretion and metabolic regulation.
- GIP Receptor (GIPR)
- A receptor activated by GIP that influences insulin secretion and energy balance.
- Dual Agonist
- A compound designed to activate two different receptors simultaneously.
- Triple Agonist
- A compound engineered to activate three receptors, often GLP-1, GIP, and glucagon receptors.
- Multi-Agonist
- A peptide or compound that targets multiple receptor pathways to produce synergistic effects.
- Insulin Secretion
- The release of insulin from pancreatic beta cells in response to glucose or hormonal signaling.
- Gastric Emptying
- The rate at which stomach contents pass into the small intestine; often slowed by GLP-1 signaling.
- Appetite Regulation
- Neurohormonal processes that control hunger, satiety, and food intake.
- Energy Balance
- The relationship between energy intake (food) and energy expenditure.
- Glycemic Control
- The regulation of blood glucose levels within a target range.
- Insulin Sensitivity
- The efficiency with which cells respond to insulin signaling.
- Beta Cell Function
- The ability of pancreatic beta cells to produce and secrete insulin.
- Glucose Homeostasis
- Maintenance of stable blood glucose levels through hormonal coordination.
- Incretin Effect
- The enhanced insulin response observed when glucose is ingested orally versus intravenously.
- Receptor Selectivity
- The degree to which a compound preferentially activates one receptor over others.
- Metabolic Signaling
- Cellular communication pathways that regulate energy storage, utilization, and glucose metabolism.