The pancreas produces several hormones, but two dominate: insulin and glucagon. These two hormones work in opposition to keep your blood sugar within a tight range, roughly 70 to 110 mg/dL. A handful of other hormones, including somatostatin and small amounts of ghrelin, are also made in the pancreas, though their roles are more specialized.
What makes the pancreas unusual is that most of it has nothing to do with hormones at all. About 95% of pancreatic tissue produces digestive enzymes that break down food in your small intestine. The remaining 5% is made up of tiny clusters of hormone-producing cells called the islets of Langerhans, and these are where all the endocrine action happens.
Insulin: The Blood Sugar Lowering Hormone
Insulin is produced by beta cells inside the islets of Langerhans. When your blood sugar rises after a meal, beta cells detect the increase and release insulin into the bloodstream. Insulin’s primary job is to help your body’s cells absorb glucose from the blood so they can use it for energy. It works by triggering glucose transporters to move to the surface of muscle and fat cells, essentially opening doors that let sugar flow in. Without this signal, glucose stays trapped in the bloodstream.
Insulin also tells the liver to stop releasing stored sugar and to start packing excess glucose away for later use. This combination of pulling sugar into cells and shutting off the liver’s glucose output is what brings blood sugar back down after eating. A fasting blood sugar below 100 mg/dL is considered normal. Between 100 and 125 mg/dL falls in the prediabetic range, and 126 mg/dL or higher on two separate tests indicates diabetes.
Interestingly, insulin doesn’t act alone in response to meals. Hormones released by your gut, called incretins, amplify insulin secretion after you eat. These gut signals account for 50% to 70% of the insulin released after a meal. This is why the same amount of glucose triggers a much larger insulin response when eaten than when injected directly into the bloodstream. Medications like tirzepatide, used for type 2 diabetes and weight management, mimic these gut hormones to boost the pancreas’s natural insulin output.
Glucagon: The Blood Sugar Raising Hormone
Glucagon is produced by alpha cells, which make up about 20% of each islet. It does the opposite of insulin. When blood sugar drops too low, whether from fasting, prolonged exercise, or simply going several hours without food, alpha cells release glucagon to bring levels back up.
Glucagon raises blood sugar through several pathways. It signals the liver to break down its stored form of glucose (glycogen) and release it into the bloodstream. If glycogen stores are running low, glucagon tells the liver to build new glucose from amino acids and other raw materials. It also triggers the breakdown of stored fat, releasing components that the liver can convert into glucose. All three of these processes work together to prevent blood sugar from falling dangerously low between meals or during physical activity.
Protein-rich meals also stimulate glucagon release. This makes sense: a meal high in protein but low in carbohydrates still triggers insulin (because amino acids stimulate beta cells), so glucagon rises in parallel to prevent blood sugar from crashing.
How Insulin and Glucagon Work Together
These two hormones function like a thermostat. After a carbohydrate-heavy meal, blood sugar climbs, insulin rises, and glucagon falls. Between meals or during a long workout, blood sugar dips, glucagon rises, and insulin drops. This push-pull dynamic keeps glucose levels remarkably stable throughout the day.
When this system breaks down, the consequences are significant. In type 1 diabetes, the immune system destroys beta cells, so the pancreas can no longer produce insulin. In type 2 diabetes, cells gradually stop responding to insulin’s signal, and beta cells eventually can’t keep up with demand. In both cases, blood sugar rises unchecked. Less commonly, tumors called insulinomas cause beta cells to overproduce insulin, leading to episodes of dangerously low blood sugar with symptoms like dizziness, blurred vision, and confusion. Glucagonomas, tumors of the alpha cells, cause excess glucagon and can lead to weight loss, skin rashes, and elevated blood sugar.
Somatostatin: The Braking Hormone
Delta cells in the islets produce somatostatin, a hormone that acts as a brake on the system. Within the pancreas, somatostatin inhibits the release of both insulin and glucagon, preventing either one from overshooting. It also suppresses digestive enzymes produced by the pancreas’s exocrine tissue.
Somatostatin’s influence extends well beyond the pancreas. In the gut, it slows gastric secretion and limits other digestive hormones. In the brain, it blocks the pituitary gland from releasing growth hormone, thyroid-stimulating hormone, and prolactin. It functions as a widespread “slow down” signal across multiple organ systems, fine-tuning hormonal output so the body doesn’t overreact to any single stimulus.
Other Hormones From the Pancreas
The pancreas also produces small amounts of ghrelin, a hormone better known for its role in hunger signaling. Your stomach is the main source of ghrelin, but pancreatic tissue contributes a small portion. Beyond triggering appetite, ghrelin stimulates the pancreas’s own alpha cells to release glucagon, creating another link between hunger and blood sugar regulation.
Beta cells also co-release amylin alongside insulin after meals. Amylin slows the rate at which food empties from the stomach and suppresses glucagon secretion, both of which help prevent blood sugar from spiking too quickly. It works as a complement to insulin, smoothing out the post-meal glucose curve rather than lowering it directly.
Pancreatic polypeptide is another hormone produced in the islets, released after eating. It helps regulate the rate of digestive enzyme secretion and may play a role in appetite control, though its effects are subtler and less well understood than those of the major hormones.
Why Such a Small Amount of Tissue Matters So Much
The fact that only 5% of pancreatic tissue handles all of this hormonal regulation underscores how efficient the islet system is. Roughly one to two million islets are scattered throughout the pancreas, each one a self-contained unit with alpha, beta, and delta cells communicating with each other in real time. The close physical proximity of these cells allows them to fine-tune each other’s output almost instantly, responding to changes in blood sugar within minutes.
This architecture also explains why damage to even a small portion of the pancreas can have outsized effects on blood sugar control. Chronic pancreatitis, autoimmune destruction, or surgical removal of pancreatic tissue can all impair islet function and lead to diabetes, even when the vast majority of the organ’s digestive tissue remains intact.