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Delta cell
Delta cell
Delta cell
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Delta cell
Control of stomach acid
Details
LocationStomach, intestine and the pancreatic islets
FunctionSomatostatin production
Identifiers
Latinendocrinocytus D
THH3.04.02.0.00027
FMA62935
Anatomical terms of microanatomy

Delta cells (δ-cells or D cells) are somatostatin-producing cells. They can be found in the stomach, intestine and the pancreatic 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 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.[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 inhibiting insulin release.[5] Viewed under an electron microscope, delta-cells can be identified as cells with smaller and slightly more compact granules than beta cells.[6]

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

[edit]

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 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).[7] 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.[8]

See also

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Delta cell

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from Grokipedia
Delta cells, also known as δ-cells, are endocrine cells that produce and secrete somatostatin, a peptide hormone that acts primarily as an inhibitor of various physiological processes. Found in the pancreatic islets of Langerhans (comprising approximately 5% of islet cells), the gastrointestinal tract (as D-cells), and the central nervous system including the hypothalamus, delta cells play a key role in regulating hormone release and digestive functions. In the pancreas, somatostatin secreted by delta cells functions as a paracrine signal, inhibiting the release of insulin from β-cells and glucagon from α-cells to maintain glucose homeostasis. This inhibitory action extends to other secretions, including gastrointestinal hormones like gastrin and secretin, pancreatic enzymes, and growth hormone from the pituitary gland. Pancreatic delta cells are electrically excitable and exhibit complex morphology with long processes that facilitate local communication within the islets. Their somatostatin secretion is stimulated by elevated glucose levels (beginning at around 3 mM and increasing with higher concentrations), certain amino acids such as leucine and arginine, and other factors like GABA, while it is inhibited by free fatty acids like palmitate. In human islets, delta cells are distributed throughout the structure, unlike in rodents where they are more confined to the periphery, influencing species-specific differences in islet regulation. Beyond the , delta cells in the (D-cells) contribute to about 65% of the body's production, helping to control secretion, intestinal motility, and nutrient absorption by suppressing exocrine and endocrine outputs. In the , from delta-like cells modulates , formation, and neuronal excitability. Dysfunctions in delta cells have been implicated in metabolic disorders; for instance, in , altered delta cell function contributes to impaired suppression and dysregulated insulin release, potentially exacerbating and responses. Research continues to explore therapeutic targets, such as antagonists, to restore delta cell-mediated control in disease states.

Anatomy and Distribution

In the Pancreas

Delta cells, also known as δ-cells, constitute approximately 5-10% of the endocrine cell population within human pancreatic islets of Langerhans. These cells are scattered throughout the islets in humans, often positioned more frequently at the periphery, with elongated processes extending toward the central β-cell core and adjacent capillaries to facilitate intercellular communication. In contrast, the distribution of delta cells varies across species; in , they are predominantly located in the peripheral of the islets, surrounding the central β-cell . Delta cells were first morphologically identified in islets by Warren Bloom in 1931 using histological staining techniques, distinguishing them as a distinct granulated separate from α- and β-cells. Their association with somatostatin secretion was later confirmed in the 1970s through pioneering immunohistochemical studies by researchers including Julia M. Polak and Stephen R. Bloom, which localized the to these cells. Recent investigations as of 2025 have revealed alterations in delta cell architecture in diabetic conditions, particularly in type 1 diabetes, where islets exhibit islet remodeling with approximately a twofold increase in direct contacts between delta cells and α-cells compared to non-diabetic pancreata.

In the Gastrointestinal Tract

Delta cells, also known as D cells, are somatostatin-producing enteroendocrine cells distributed throughout the gastrointestinal (GI) tract mucosa, with notable presence in the gastric antrum, duodenum, and extending into the small and large intestines. In the stomach, they are primarily located in the pyloric antrum, where they interact closely with neighboring G cells and enterochromaffin-like cells to modulate gastric acid secretion. Further along the GI tract, delta cells populate the duodenal mucosa and are scattered across the jejunum, ileum, and colonic epithelium, contributing to local regulation of nutrient absorption and motility. Their distribution is not uniform, with higher densities observed in proximal regions such as the duodenum compared to more distal sites like the ileum and colon. In terms of relative abundance, delta cells comprise approximately 17-20% of the endocrine cell population in the gastric antrum of healthy individuals, though this proportion can vary with conditions like infection, which may reduce their numbers. Overall, they account for about 3-5% of total enteroendocrine cells across the lower GI tract, making them one of the less common subtypes, particularly in the colon and where they are evenly dispersed but sparse. These cells exhibit a spindle-shaped morphology, often with an apical extension sensing luminal contents and a basal process facilitating release directly into the bloodstream; they are typically clustered within mucosal glands and in proximity to other enteroendocrine cells, enabling networks. Delta cells demonstrate evolutionary conservation across vertebrates, with somatostatin-expressing cells identifiable in species from agnathans to mammals, underscoring their ancient role in gut regulation. This preservation is evident in their consistent mucosal localization and higher proximal gut density, a pattern observed from to humans, which supports coordinated inhibition of digestive processes in response to environmental and dietary cues.

Cellular Structure

Morphology

Delta cells exhibit an elongated, spindle-shaped morphology, characterized by a well-defined cell soma and long cytoplasmic processes that resemble dendrites or , extending up to 10-20 μm in length. These processes enable the cells to adopt a neuron-like appearance, facilitating close contacts with multiple neighboring endocrine cells, such as alpha and beta cells, as well as vascular structures within the . The overall cell diameter typically measures 10-15 μm, with an eccentric nucleus positioned within the . Under light microscopy, delta cells display positive staining with silver impregnation techniques, historically used to identify them as argyrophilic A1 cells due to the deposition of silver in their secretory granules. Electron microscopy reveals their distinctive dense-core secretory granules, which appear as electron-dense structures containing somatostatin and measure approximately 200-350 nm in diameter. Morphological differences exist across species; in rodents, delta cells often show more extensive interconnections through prominent cytoplasmic extensions, contributing to a highly branched network in the islet periphery, whereas in humans, they appear more compact with fewer projections and are dispersed throughout the islet core.

Molecular Markers

Delta cells are primarily identified by the expression of the somatostatin (SST) gene, which encodes the somatostatin, a hallmark of their identity across both pancreatic and gastrointestinal contexts. Transcriptomic analyses confirm high SST mRNA levels selectively in delta cells, distinguishing them from other islet endocrine populations. The mature SST peptide is stored in secretory granules and serves as the definitive intracellular marker for delta cell identification. Differentiation of delta cells during pancreatic development involves key transcription factors, including the aristaless-related homeobox (Arx) and paired box 6 (). Arx contributes to the specification of endocrine subtypes by repressing alternative lineages, with its absence leading to expanded delta cell populations alongside beta cells. regulates SST gene transcription and is essential for the maturation of delta cells, as evidenced by reduced somatostatin expression in -deficient models. These factors operate within a network that ensures proper endocrine lineage commitment. On the cell surface, delta cells express subtypes, notably SSTR2 and SSTR5, which mediate autocrine inhibition of release. SSTR5 predominates in delta cells, colocalizing with SST in approximately 75% of these cells, while SSTR2 is also present to facilitate local feedback signaling. Both subtypes are G-protein-coupled receptors that contribute to paracrine regulation within islets. Additional identifiers include co-expression of in delta cells, particularly noted in pancreatic populations and extending to some gastrointestinal delta cells where it modulates local signaling. Delta cells are consistently negative for insulin gene (INS) expression, providing a clear distinction from insulin-producing beta cells in transcriptomic and histological studies. For diagnostic and research purposes, using anti-SST antibodies reliably detects delta cells in tissue sections from and , enabling precise localization and quantification. In flow cytometry applications, surface markers such as LY6H or combinations including , CD49f, and CD71 allow for the isolation of viable delta cells from dissociated islets with high purity.

Physiology

Somatostatin Secretion

Somatostatin is biosynthesized in delta cells from a precursor known as preprosomatostatin, a 116-amino-acid polypeptide encoded by the SST gene. This precursor undergoes post-translational processing, including signal peptide cleavage to form prosomatostatin (92 amino acids), followed by enzymatic cleavage at dibasic residues by prohormone convertases such as PC1/3 and PC2, yielding the mature cyclic peptides somatostatin-14 (SST-14) and somatostatin-28 (SST-28). SST-14, comprising the C-terminal 14 amino acids, is the predominant isoform in pancreatic delta cells, while SST-28, which includes an N-terminal extension of 14 additional amino acids, prevails in delta cells of the gastrointestinal tract. The mature somatostatin isoforms are concentrated and stored in dense-core secretory granules within the cytoplasm of delta cells. These granules, typically measuring 100-200 nm in diameter, exhibit an electron-dense core surrounded by a halo and are formed through the regulated secretory pathway in the trans-Golgi network. Storage in these granules allows for rapid mobilization upon stimulation, with release occurring exclusively via rather than constitutive . Somatostatin secretion from delta cells is mediated by calcium-dependent of these secretory granules. Upon elevation of intracellular Ca²⁺ levels, typically triggered by activation, the granules dock and fuse with the plasma membrane through SNARE complex formation involving proteins such as syntaxin-1A, SNAP-25, and VAMP2. This process ensures precise control over hormone release, with SST-14 being the primary form secreted from pancreatic delta cells under physiological conditions. The released exerts paracrine effects on neighboring cells to modulate their activity.

Regulatory Roles

Delta cells exert significant regulatory influence through the paracrine and endocrine actions of (SST), primarily modulating hormone secretion in the , pituitary, and . Within , SST secreted by delta cells provides a tonic paracrine inhibition of insulin release from beta cells and release from alpha cells, preventing excessive hormonal output and facilitating coordinated islet responses to nutrient stimuli. This inhibition occurs via somatostatin receptors (SSTRs), primarily SSTR2 in human islets mediating suppression of both insulin secretion in beta cells and in alpha cells, with SSTR5 contributing to insulin inhibition. Recent studies as of 2025 in human islets emphasize SSTR2's dominant role in coordinating paracrine inhibition of insulin and , highlighting species-specific differences from . Somatostatin exerts endocrine regulation, primarily from hypothalamic sources, by inhibiting the release of (GH) and (TSH) from the , thereby influencing systemic and function. This hypothalamic-pituitary axis modulation helps maintain hormonal balance, with SST acting as a key brake on excessive GH and TSH in response to various physiological signals. In the gastrointestinal tract, delta cell-derived SST exerts paracrine and endocrine effects that inhibit the of from G cells and from S cells, while also suppressing production, pepsinogen release, and overall gut to regulate and absorption. These regulatory roles are crucial for fine-tuning glucose , as SST from delta cells curbs over-secretion of and during meals, ensuring precise adjustments to blood glucose levels and preventing or . In humans, the intermixed distribution of delta cells throughout the islets—unlike the more segregated peripheral positioning in —enhances strength, allowing for more direct and potent inhibition of neighboring beta and alpha cells to support robust metabolic control.

Regulation of Delta Cell Activity

Stimuli for Secretion

Delta cells respond to various physiological stimuli that trigger the secretion of , primarily through mechanisms involving , calcium influx, and cyclic AMP (cAMP) signaling. These stimuli ensure coordinated regulation of islet hormone release during absorption and metabolic demands. , hormonal, neural, , and circadian factors each contribute to enhancing output from delta cells in the and . Responses may vary between species, with delta cells showing distributed regulation unlike peripheral confinement in . Nutrient stimuli, particularly elevated glucose levels, directly promote somatostatin secretion. Glucose concentrations above 3 mM depolarize delta cells by facilitating , leading to increased ATP production and closure of ATP-sensitive (KATP) channels, which in turn opens voltage-gated calcium channels and triggers . Although GLUT2 is a key facilitator of glucose uptake in beta cells, delta cells primarily utilize and SGLT2 for this process, with SGLT2 contributing to intracellular sodium elevation that further boosts via the mitochondrial sodium-calcium exchanger. This glucose-dependent response occurs in a dose-dependent manner, with significant stimulation observed from 3 mM onward, saturating above 10 mM in both and islets. Postprandial increases in glucose thus enhance release to fine-tune insulin and secretion. Hormonal signals from the gut, such as (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), potently stimulate delta cell activity during meals. GLP-1 binds to GLP-1 receptors on delta cells, activating Gs-coupled pathways that elevate cAMP levels, potentiate calcium-induced calcium release, and amplify independently of changes. Similarly, GIP acts via its receptors to increase cAMP and enhance somatostatin output, contributing to postprandial suppression of . These incretins, released from enteroendocrine cells in response to nutrient ingestion, ensure timely paracrine inhibition within islets. Neural inputs, especially from the , provide rapid stimulation of secretion. Vagal stimulation releases , which binds to muscarinic M1 or M3 receptors on delta cells, mobilizing intracellular calcium stores and increasing calcium influx through voltage-gated channels. This pathway heightens delta cell responsiveness during the cephalic phase of , promoting release to coordinate overall function. can also originate paracrine-like from alpha cells, further amplifying this effect in human islets. Certain serve as direct stimulators of secretion, particularly and during protein-rich meals. induces through electrogenic transport via cationic amino acid transporters (e.g., SLC7A5), leading to calcium entry and . , metabolized to α-ketoisocaproate, boosts ATP production via the tricarboxylic acid cycle, closing KATP channels and mimicking glucose effects. These , at physiological concentrations (e.g., 10 mM or ), elicit robust release from isolated islets or perfused , underscoring their role in nutrient sensing by delta cells. Circadian rhythms modulate somatostatin secretion, with peaks occurring during the fed state to align with daily metabolic cycles. Clock genes such as PER2 regulate this temporal pattern in delta cells, influencing and secretory responsiveness to nutrients. Disruptions in circadian alignment, as seen in or clock gene mutations, can dampen these peaks, affecting coordination. This rhythmic control ensures somatostatin output synchronizes with feeding-fasting transitions, optimizing glucose over 24-hour periods.

Feedback Mechanisms

Delta cells employ multiple feedback mechanisms to regulate somatostatin (SST) secretion, ensuring precise control over islet hormone dynamics and preventing dysregulation of glucose homeostasis. A key autocrine mechanism involves SST binding to somatostatin receptor types 1 and 3 (SSTR1 and SSTR3) expressed on the delta cell membrane, which inhibits further SST release and restrains uncontrolled secretion. This negative loop is mediated through G-protein-coupled signaling that hyperpolarizes the cell and suppresses exocytosis, thereby maintaining balanced paracrine inhibition within the islet. SSTR1 and SSTR3 are highly expressed in delta cells, underscoring their central role in this self-regulatory process. Paracrine feedback from neighboring beta cells further modulates delta cell activity, with insulin proposed to suppress SST secretion via insulin receptors on delta cells, though evidence is mixed. This interaction is crucial during , as elevated insulin levels may dampen delta cell responsiveness, reducing SST-mediated inhibition of both insulin and release to support appropriate glycemic control. Studies in isolated islets have demonstrated insulin's potential to inhibit glucose-stimulated SST secretion in some models, highlighting bidirectional communication, while others show no direct effect. Hormonal signals from , including and , exert effects on delta cell activity to integrate systemic metabolic status. , acting through its receptors on delta cells, stimulates SST secretion by elevating Ca2+ via PKC activation, indirectly limiting insulin output and contributing to energy balance. similarly influences islet regulation, promoting metabolic by modulating endocrine responses, including potential effects on SST output during chronic high-fat conditions. At low glucose concentrations, delta cells undergo hyperpolarization primarily via activation of ATP-sensitive (KATP) channels, which increases efflux, stabilizes the , and reduces calcium influx necessary for SST . This intrinsic feedback minimizes SST secretion during , thereby avoiding suppression of release from alpha cells and facilitating counterregulation. Gap junctions between beta and delta cells propagate this hyperpolarization, amplifying the effect across the islet. In pathophysiological states like , feedback mechanisms in delta cells adapt to prevent ensuing , with upregulated SST signaling serving to curtail excessive insulin secretion from beta cells. Morphological and functional changes in delta cells, such as increased connectivity or receptor sensitivity, enhance this inhibitory loop, compensating for dysregulated communication in or . However, in advanced , impaired delta cell feedback exacerbates glycemic instability, underscoring the adaptive role of these mechanisms in metabolic resilience.

Pathophysiology and Clinical Relevance

Role in Metabolic Disorders

In , autoimmune destruction primarily targets beta cells, with delta cell mass remaining relatively preserved. However, levels are elevated, contributing to impaired counterregulation during . This altered somatostatin signaling, along with loss of insulin-mediated suppression, allows inappropriate secretion during . Studies in human pancreatic tissues from long-standing patients reveal remodeled delta-cell architecture, including altered intra-islet positioning, but elevated SST signaling impairs appropriate suppression during . In , delta cells often exhibit and structural remodeling, such as increased cellular processes and from alpha cells, as observed in models; human studies show increased delta cell proportions in some cohorts but lack confirmation of alpha-to-delta . For instance, in the Goto-Kakizaki model of , delta cell numbers rise progressively with age, accompanied by elevated SST mRNA expression. However, this compensatory increase is coupled with impaired delta-cell responsiveness to glucose fluctuations, resulting in dysregulated SST secretion that fails to appropriately modulate insulin and outputs, contributing to glycemic instability. In obesity, islet SST levels are elevated, as evidenced by hypersecretion from obese Zucker rat islets under various glucose conditions, which correlates with enhanced insulin resistance by potentiating peripheral metabolic impairments and reducing insulin sensitivity. Therapeutic strategies targeting delta cells involve SST analogs like , which modulate islet hormone secretion in . In , suppresses both insulin and glucagon release, stabilizing glucose without significant lowering, while in insulin-dependent cases, it enhances insulin sensitivity and reduces requirements. These analogs offer potential for addressing delta-cell dysregulation, though side effects like gastrointestinal issues limit widespread use.

Associated Tumors

Somatostatinomas are rare neuroendocrine tumors originating from , which produce excessive , leading to distinct clinical manifestations. These tumors most commonly arise in the or , with pancreatic somatostatinomas frequently located in the head of the organ. They account for less than 1% of all gastroenteropancreatic neuroendocrine tumors. The annual incidence is estimated at 1 in 40 million individuals. Approximately 35-45% of pancreatic somatostatinomas are associated with () syndrome, a hereditary condition predisposing to various endocrine tumors. The hallmark of somatostatinoma is the somatostatinoma syndrome, resulting from somatostatin excess, which inhibits insulin and secretion (causing diabetes mellitus), gallbladder contractility (leading to cholelithiasis or ), and pancreatic exocrine function (resulting in and ). Additional symptoms may include , hypochlorhydria, , , or , though the full syndrome is present in fewer than 5% of cases, as many tumors are non-functional or until advanced. Diagnosis involves measuring elevated fasting plasma somatostatin levels, typically exceeding 30 pg/mL (above the normal range of less than 30 pg/mL), to confirm hypersecretion. Imaging modalities such as computed tomography (CT), magnetic resonance imaging (MRI), or positron emission tomography (PET) with gallium-68 somatostatin analogs localize the tumor, while endoscopic ultrasound aids in smaller lesions. Definitive confirmation requires biopsy, demonstrating somatostatin-positive cells via immunohistochemistry and assessing tumor grade with Ki-67 proliferation index. Treatment prioritizes surgical resection for localized disease, offering the only potential cure, particularly for duodenal tumors amenable to endoscopic or Whipple procedures. For metastatic or unresectable cases, like or paradoxically control symptoms by binding tumor receptors to suppress further release and stabilize tumor growth. Additional options include (PRRT), targeted agents such as , or in aggressive scenarios.

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