glucagon-like peptide-1 (GLP-1)
GLP-1 is the gut hormone behind some of the most talked-about modern weight and diabetes medicines. After you eat, intestinal cells release it, and it acts like a multi-purpose “meal-handling manager”: it boosts insulin, calms the rival hormone glucagon, slows the stomach, and tells the brain you are full.
Made by L-cells in the lower small intestine and colon, GLP-1 is one of the two main incretins. Its insulin-boosting action is glucose-dependent — it only pushes insulin when blood sugar is elevated — which makes it safer regarding low-sugar episodes than older drugs. It also suppresses glucagon secretion from pancreatic alpha cells, slows gastric emptying so glucose enters the blood more gradually, and acts on appetite centers in the hypothalamus to reduce hunger.
Native GLP-1 is destroyed within minutes by the enzyme DPP-4. Drug developers solved this by making long-lasting GLP-1 receptor agonists (such as semaglutide and liraglutide) that resist degradation, giving sustained glucose-lowering and substantial weight loss. These are now used both for type 2 diabetes and for obesity.
An honest caveat: the appetite and weight effects come partly from delayed gastric emptying and central action, and the most common side effects are gastrointestinal — nausea, vomiting, and constipation — especially when the dose is increased.
A person with type 2 diabetes on a weekly GLP-1 receptor agonist injection eats smaller portions, feels full sooner, and sees both blood glucose and body weight fall over several months.
GLP-1 receptor agonists lower glucose and reduce appetite.
“Glucagon-like” refers to its structure: GLP-1 is cut from the same precursor protein (proglucagon) as glucagon, yet its actions on blood sugar are largely opposite.