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The Appetite Hormone Map: Ghrelin, Leptin, PYY, GLP-1, CCK, Amylin and the Brain
Hunger is not one signal. It is a conversation among the gut, fat tissue, pancreas and brain, with different hormones speaking at different times and over different time scales. This map lays out the main voices.
Key takeaways
- Short-term signals come from the gut around each meal.
- Long-term signals from fat and the pancreas report the body’s stores.
- The hypothalamus and brainstem integrate them.
- Many research compounds mimic or block one of these hormones.
Short-term: the meal signals
- Ghrelin (stomach). Rises before meals and falls after eating. It stimulates appetite and growth hormone release (see the story of ghrelin).
- CCK (cholecystokinin, from the duodenum). Released in response to fat and protein, acts partly through the vagus nerve to end a meal.
- GLP-1 (L cells in the lower intestine). Released after eating, boosts insulin in a glucose-dependent way, slows gastric emptying and acts on the brain to reduce intake (see the incretin story).
- PYY (L cells). The form PYY(3-36) rises after meals and reduces appetite through Y2 receptors.
- GIP (K cells in the upper intestine). The other incretin, with roles in insulin and fat metabolism.
- Oxyntomodulin activates both the GLP-1 and glucagon receptors.
Medium and long-term: the stores
- Insulin (pancreatic beta cells). Rises with feeding and acts in the brain as an adiposity signal.
- Amylin (co-secreted with insulin). Contributes to meal-ending signals and slows stomach emptying.
- Leptin (fat cells). Proportional to fat stores, signals long-term energy status (see the story of leptin).
The brain: where it comes together
The arcuate nucleus of the hypothalamus contains two opposing neuron types. NPY/AgRP neurons stimulate appetite, while POMC/CART neurons suppress it by releasing alpha-MSH onto MC4R (see the agouti mouse story). Ghrelin activates the first group, and leptin and insulin inhibit the first and activate the second. Signals also reach the brainstem, particularly the nucleus of the solitary tract, which receives vagal input from the gut. Reward and emotional circuits add further influence beyond homeostasis.
Timing diagram in words
- Before a meal: ghrelin up, GLP-1 and PYY low.
- During a meal: CCK and vagal signals rise.
- After a meal: GLP-1, PYY and insulin peak, ghrelin falls.
- Over weeks: leptin tracks fat mass, and drops with weight loss (see why weight loss plateaus).
Why the map matters for research
Each hormone is a potential target. Single-receptor agonists, dual agonists and triple agonists differ in which parts of this map they engage. Reading a paper means asking which receptors a compound hits and in which tissues (see receptor maps for the melanocortin branch).
The bottom line
Appetite is a distributed system with redundancy, which is why single interventions often meet compensation. The more of the map you understand, the easier it is to see why results look the way they do.
Related reading
- The Story of Ghrelin: A Receptor Looking for a Hormone
- The Story of Leptin: A Fat Mouse, a Surgical Experiment and a Missing Hormone
- From the Incretin Effect to GLP-1: How a Gut Hormone Was Found
- Browse the full Research Library
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For laboratory research use only. Not for human or veterinary use, and not intended to diagnose, treat, cure or prevent any condition. This article is educational and is not medical advice.