View source for Delta cell

{{Short description|Somatostatin-producing cell}}
{{distinguish|D battery}}
{{Infobox cell
| Name        = Delta cell
| Latin       = endocrinocytus D
| Image       = Control-of-stomach-acid-sec.png
| Caption     = Control of stomach acid
| Image2      =
| Caption2    =
| Precursor   =
| Location = [[Stomach]], [[intestine]] and the [[pancreatic islet]]s
| Function = [[Somatostatin]] production
}}

'''Delta cells''' ('''δ-cells''' or '''D cells''') are [[somatostatin]]-producing [[cell (biology)|cell]]s. They can be found in the [[stomach]], [[intestine]] and the [[pancreatic islet]]s. Delta cells comprise ca 5% of the cells in the islets<ref>{{cite journal | vauthors = Cabrera O, Berman DM, Kenyon NS, Ricordi C, Berggren PO, Caicedo A | title = The unique cytoarchitecture of human pancreatic islets has implications for islet cell function | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 103 | issue = 7 | pages = 2334–2339 | date = February 2006 | pmid = 16461897 | pmc = 1413730 | doi = 10.1073/pnas.0510790103 | bibcode = 2006PNAS..103.2334C | doi-access = free }}</ref> 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.<ref>{{cite journal | vauthors = Brereton MF, Vergari E, Zhang Q, Clark A | title = Alpha-, Delta- and PP-cells: Are They the Architectural Cornerstones of Islet Structure and Co-ordination? | journal = The Journal of Histochemistry and Cytochemistry | volume = 63 | issue = 8 | pages = 575–591 | date = August 2015 | pmid = 26216135 | pmc = 4530398 | doi = 10.1369/0022155415583535 }}</ref> In both species, the peptide hormone [[Urocortin 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.<ref>{{cite journal | vauthors = van der Meulen T, Donaldson CJ, Cáceres E, Hunter AE, Cowing-Zitron C, Pound LD, Adams MW, Zembrzycki A, Grove KL, Huising MO | display-authors = 6 | title = Urocortin3 mediates somatostatin-dependent negative feedback control of insulin secretion | journal = Nature Medicine | volume = 21 | issue = 7 | pages = 769–776 | date = July 2015 | pmid = 26076035 | pmc = 4496282 | doi = 10.1038/nm.3872 }}<!--|access-date=2016-05-30--></ref> It has also been suggested that somatostatin may be implicated in insulin-induced hypoglycaemia through a mechanism involving SGLT-2 receptors.<ref>{{cite journal | vauthors = Vergari E, Knudsen JG, Ramracheya R, Salehi A, Zhang Q, Adam J, Asterholm IW, Benrick A, Briant LJ, Chibalina MV, Gribble FM, Hamilton A, Hastoy B, Reimann F, Rorsman NJ, Spiliotis II, Tarasov A, Wu Y, Ashcroft FM, Rorsman P | display-authors = 6 | title = Insulin inhibits glucagon release by SGLT2-induced stimulation of somatostatin secretion | journal = Nature Communications | volume = 10 | issue = 1 | page = 139 | date = January 2019 | pmid = 30635569 | pmc = 6329806 | doi = 10.1038/s41467-018-08193-8 | bibcode = 2019NatCo..10..139V | doi-access = free }}</ref> [[Ghrelin]] can also strongly stimulate somatostatin secretion, thus indirectly inhibiting [[insulin]] release.<ref>{{cite journal | vauthors = DiGruccio MR, Mawla AM, Donaldson CJ, Noguchi GM, Vaughan J, Cowing-Zitron C, van der Meulen T, Huising MO | display-authors = 6 | title = Comprehensive alpha, beta and delta cell transcriptomes reveal that ghrelin selectively activates delta cells and promotes somatostatin release from pancreatic islets | journal = Molecular Metabolism | volume = 5 | issue = 7 | pages = 449–458 | date = July 2016 | pmid = 27408771 | pmc = 4921781 | doi = 10.1016/j.molmet.2016.04.007 }}</ref> Viewed under an [[electron microscope]], delta-cells can be identified as cells with smaller and slightly more compact [[Granule (cell biology)|granules]] than [[beta cell]]s.<ref>{{cite journal | vauthors = Rorsman P, Huising MO | title = The somatostatin-secreting pancreatic δ-cell in health and disease | journal = Nature Reviews. Endocrinology | volume = 14 | issue = 7 | pages = 404–414 | date = July 2018 | pmid = 29773871 | pmc = 5997567 | doi = 10.1038/s41574-018-0020-6 }}</ref>

The δ-cells in the stomach contain [[CCKBR]] (which respond to gastrin) and [[M3 receptors]] (which respond to Ach). Respectively, these receptors will increase [[somatostatin]] 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-producing [[parietal 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, including [[gastrin]], [[secretin]] and [[histamine]] which effectively slows down the digestive process.

==Clinical significance==
A tumor of the delta cells is called a "[[somatostatinoma]]".

When a person is infected with ''[[H. pylori]]'' the lower region of the stomach, the [[Pyloric antrum|antrum]], is predominantly inflamed. This is where most of the δ-cells in the stomach are. The bacteria produce a cloud of ammonia around themselves using [[urease]] 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 low [[PD-L1]] expression on the δ-cells as compared to gastric G cells (resulting in higher susceptibility of δ-cells to inflammatory responses).<ref>{{cite journal | vauthors = Mommersteeg MC, Yu BT, van den Bosch TP, von der Thüsen JH, Kuipers EJ, Doukas M, Spaander MC, Peppelenbosch MP, Fuhler GM | title = Constitutive programmed death ligand 1 expression protects gastric G-cells from Helicobacter pylori-induced inflammation | journal = Helicobacter | volume = 27 | issue = 5 | article-number = e12917 | date = October 2022 | pmid = 35899973 | doi = 10.1111/hel.12917| pmc = 9542424 }}</ref> In turn, this results in a lower level of [[somatostatin]] being secreted and consequently higher release of [[gastrin]] and stomach acid. This, combined with the damage from ammonium, leads to ulceration of the stomach wall.<ref>{{cite journal | vauthors = Liu Y, Vosmaer GD, Tytgat GN, Xiao SD, Ten Kate FJ | title = Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori associated and non-associated gastritis | journal = Journal of Clinical Pathology | volume = 58 | issue = 9 | pages = 927–931 | date = September 2005 | pmid = 16126872 | pmc = 1770830 | doi = 10.1136/jcp.2003.010710 }}</ref>

== See also ==
*[[List of human cell types derived from the germ layers]]
*[[List of distinct cell types in the adult human body]]

== References ==
{{Reflist}}{{Endocrine system anatomy}}{{Gastrointestinal physiology}}
{{Authority control}}

[[Category:Peptide hormone secreting cells]]
[[Category:Stomach]]

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