| Delta cell | |
|---|---|
 Control of stomach acid | |
| Details | |
| Location | Stomach,intestine and thepancreatic islets |
| Function | Somatostatin production |
| Identifiers | |
| Latin | endocrinocytus D |
| TH | H3.04.02.0.00027 |
| FMA | 62935 |
| Anatomical terms of microanatomy | |
Delta cells (δ-cells orD cells) aresomatostatin-producingcells. They can be found in thestomach,intestine and thepancreatic islets. Delta cells comprise ca 5% of the cells in the islets[1] but may interact with many more islet cells than suggested by their low numbers. In rodents, delta-cells are located in the periphery of the islets; in humans the islet architecture is generally less organized and delta-cells are frequently observed inside the islets as well.[2] In both species, the peptide hormoneUrocortin III (Ucn3) is a major local signal that is released from beta cells (and alpha cells in primates) to induce the local secretion of somatostatin.[3] It has also been suggested that somatostatin may be implicated in insulin-induced hypoglycaemia through a mechanism involving SGLT-2 receptors.[4]Ghrelin can also strongly stimulate somatostatin secretion, thus indirectly inhibitinginsulin release.[5] Viewed under anelectron microscope, delta-cells can be identified as cells with smaller and slightly more compactgranules thanbeta cells.[6]
The δ-cells in the stomach containCCKBR (which respond to gastrin) andM3 receptors (which respond to Ach). Respectively, these receptors will increasesomatostatin output and decrease somatostatin output from the δ-cells. VIP,vasoactive intestinal peptide, acts positively on δ-cells resulting in more somatostatin being released.
In the stomach, somatostatin acts directly on the acid-producingparietal cells via a G-protein coupled receptor (which inhibits adenylate cyclase, thus effectively antagonising the stimulatory effect of histamine) to reduce acid secretion. Somatostatin can also indirectly decrease stomach acid production by preventing the release of other hormones, includinggastrin,secretin andhistamine which effectively slows down the digestive process.
A tumor of the delta cells is called a "somatostatinoma".
When a person is infected withH. pylori the lower region of the stomach, theantrum, is predominantly inflamed. This is where most of the δ-cells in the stomach are. The bacteria produce a cloud of ammonia around themselves usingurease to protect them from the stomach acid; however, this reacts with the acid producing ammonium which is toxic to cells. This leads to many of the δ-cells dying, an effect that is further compounded by the lowPD-L1 expression on the δ-cells as compared to gastric G cells (resulting in higher susceptibility of δ-cells to inflammatory responses).[7] In turn, this results in a lower level ofsomatostatin being secreted and consequently higher release ofgastrin and stomach acid. This, combined with the damage from ammonium, leads to ulceration of the stomach wall.[8]