Pancreatic acini
Acini pancreatici
Also known as: acinar cells, exocrine pancreas
Pancreatic acini are berry-like clusters of serous acinar cells that make and secrete the digestive enzymes of pancreatic juice. Most of these enzymes are released as inactive zymogens.
Overview
Acinar cells are pyramidal. Their basal cytoplasm is densely basophilic from extensive rough ER, and their apical cytoplasm holds eosinophilic zymogen granules. They have one of the highest rates of protein synthesis in the body.
Proteases and phospholipase are stored and secreted as inactive precursors: trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidases and prophospholipase. They are packaged together with pancreatic secretory trypsin inhibitor (SPINK1) as a safeguard against autodigestion. Amylase and lipase are secreted in active form.
Secretion is triggered by CCK (largely through vagovagal reflexes in humans) and acetylcholine (M3 receptors). Both act through Ca²⁺ signalling and cause exocytosis. Secretin and VIP potentiate the response through cAMP. Inside each acinus the pale centroacinar cells mark the start of the intercalated duct.
- Location
Throughout the pancreatic parenchyma, forming about 80–85% of its volume.
Anatomy
- Histology
Serous acini with intense basal basophilia and apical eosinophilic granules. Centroacinar cells appear as pale nuclei inside the acinar lumen.
Function
- Synthesise, store and secrete pancreatic digestive enzymes.
- Secretions
Trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase A and B, pancreatic α-amylase, pancreatic lipase and procolipase, prophospholipase A2, carboxyl ester lipase (cholesterol esterase), ribonuclease and deoxyribonuclease, and SPINK1.
- Regulation
Stimulated by CCK, ACh (vagal cephalic and gastric phases), secretin and VIP (potentiation). Inhibited by somatostatin and pancreatic polypeptide.
Clinical significance
Hereditary and genetic pancreatitis
Gain-of-function mutations of cationic trypsinogen (PRSS1) make trypsin resist inactivation. Loss-of-function variants of SPINK1 remove the inhibitor safeguard. Both cause recurrent acute and then chronic pancreatitis, with a high lifetime risk of pancreatic cancer.
Compiled from standard anatomy and physiology references — see the Digestive System sources. For education only; not medical advice.