Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (682 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A 14-amino acid peptide named for its ability to inhibit pituitary growth hormone release, also called somatotropin release-inhibiting factor. It is expressed in the central and peripheral nervous systems, the gut, and other organs. SRIF can also inhibit the release of thyroid-stimulating hormone; prolactin; insulin; and glucagon besides acting as a neurotransmitter and neuromodulator. In a number of species including humans, there is an additional form of somatostatin, srif-28 with a 14-amino acid extension at the N-terminal.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Somatotropin Release-Inhibiting Hormone; Somatotropin Release Inhibiting Hormone; SRIH-14; Somatostatin, Cyclic; Cyclic Somatostatin; Somatostatin-14; Somatostatin 14; Somatotropin Release-Inhibiting Factor.
Where it fits in the MeSH classification
- Broader topics
- Pituitary Hormone Release Inhibiting Hormones; Pancreatic Hormones
- Narrower topics
- Somatostatin-28
- See also
- Receptors, Somatostatin
Related concepts
Research landscape
PubMed indexes 20,670 records tagged with the MeSH heading “Somatostatin” (counts retrieved 2026-10-31). 1,522 of them (7.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 12,588 records.
Reviews account for 2,675 records (12.9%) and meta-analyses for 108. Randomized controlled trials number 499 (2.4%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 12,588 |
| 2000-2009 | 3,670 |
| 2010-2019 | 2,890 |
| 2020 onward | 1,522 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,675 | 12.9% |
| Meta-analyses | 108 | 0.5% |
| Randomized controlled trials | 499 | 2.4% |
Method: PubMed query "Somatostatin"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Somatostatin Analogs in Clinical Practice: a Review | 2020 | Review article Design not recorded in structured metadata | 188 | cc by PMID 32121432 · DOI · PMC7084228 |
| Somatostatin Analogues in the Treatment of Neuroendocrine Tumors: Past, Present and Future | 2019 | Review article Design not recorded in structured metadata | 152 | cc by PMID 31234481 · DOI · PMC6627451 |
| Insulin inhibits glucagon release by SGLT2-induced stimulation of somatostatin secretion | 2019 | Research article Design not recorded in structured metadata | 141 | cc by PMID 30635569 · DOI · PMC6329806 |
| Mutant huntingtin expression in somatostatin-positive interneurons contributes to neurophysiological and behavioral phenotypes in BACHD mice | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 41648922 · DOI · PMC13054931 |
Somatostatin Analogs in Clinical Practice: a Review [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Somatostatin analogs are an invaluable therapeutic option in the diagnosis and treatment of somatotropinomas, thyrotropinomas, and functioning and non-functioning gastroenteropancreatic neuroendocrine tumors.
- Closing excerpt
- Somatostatin analogs have also shown to be useful in the treatment of other endocrine diseases (congenital hyperinsulinism, Graves' orbitopathy, diabetic retinopathy, diabetic macular edema), non-endocrine tumors (breast, colon, prostate, lung, and hepatocellular), and digestive diseases (chronic refractory diarrhea, hepatorenal polycystosis, gastrointestinal hemorrhage, dumping syndrome, and intestinal fistula).
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (89 words)
Somatostatin analogs are an invaluable therapeutic option in the diagnosis and treatment of somatotropinomas, thyrotropinomas, and functioning and non-functioning gastroenteropancreatic neuroendocrine tumors. They should also be considered an effective and safe therapeutic alternative to corticotropinomas, gonadotropinomas, and prolactinomas resistant to dopamine agonists. Somatostatin analogs have also shown to be useful in the treatment of other endocrine diseases (congenital hyperinsulinism, Graves' orbitopathy, diabetic retinopathy, diabetic macular edema), non-endocrine tumors (breast, colon, prostate, lung, and hepatocellular), and digestive diseases (chronic refractory diarrhea, hepatorenal polycystosis, gastrointestinal hemorrhage, dumping syndrome, and intestinal fistula).
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32121432 · DOI · PMC7084228
Somatostatin Analogues in the Treatment of Neuroendocrine Tumors: Past, Present and Future [2]
Abstract reading summary — source excerpts
- Opening excerpt
- In recent decades, the incidence of neuroendocrine tumors (NETs) has steadily increased.
- Closing excerpt
- Moreover, this review highlights the clinical evidence of SSAs in monotherapy, and in combination with other treatment modalities, as applied to the antiproliferative management of neuroendocrine tumors with special attention to recent high-quality phase III trials.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (268 words)
In recent decades, the incidence of neuroendocrine tumors (NETs) has steadily increased. Due to the slow-growing nature of these tumors and the lack of early symptoms, most cases are diagnosed at advanced stages, when curative treatment options are no longer available. Prognosis and survival of patients with NETs are determined by the location of the primary lesion, biochemical functional status, differentiation, initial staging, and response to treatment. Somatostatin analogue (SSA) therapy has been a mainstay of antisecretory therapy in functioning neuroendocrine tumors, which cause various clinical symptoms depending on hormonal hypersecretion. Beyond symptomatic management, recent research demonstrates that SSAs exert antiproliferative effects and inhibit tumor growth via the somatostatin receptor 2 (SSTR2). Both the PROMID (placebo-controlled, prospective, randomized study in patients with metastatic neuroendocrine midgut tumors) and the CLARINET (controlled study of lanreotide antiproliferative response in neuroendocrine tumors) trial showed a statistically significant prolongation of time to progression/progression-free survival (TTP/PFS) upon SSA treatment, compared to placebo. Moreover, the combination of SSA with peptide receptor radionuclide therapy (PRRT) in small intestinal NETs has proven efficacy in the phase 3 neuroendocrine tumours therapy (NETTER 1) trial. PRRT is currently being tested for enteropancreatic NETs versus everolimus in the COMPETE trial, and the potential of SSTR-antagonists in PRRT is now being evaluated in early phase I/II clinical trials. This review provides a synopsis on the pharmacological development of SSAs and their use as antisecretory drugs. Moreover, this review highlights the clinical evidence of SSAs in monotherapy, and in combination with other treatment modalities, as applied to the antiproliferative management of neuroendocrine tumors with special attention to recent high-quality phase III trials.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31234481 · DOI · PMC6627451
Insulin inhibits glucagon release by SGLT2-induced stimulation of somatostatin secretion [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Hypoglycaemia (low plasma glucose) is a serious and potentially fatal complication of insulin-treated diabetes.
- Closing excerpt
- We propose that SSTR or SGLT2 antagonists should be considered as adjuncts to insulin in diabetes therapy.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (146 words)
Hypoglycaemia (low plasma glucose) is a serious and potentially fatal complication of insulin-treated diabetes. In healthy individuals, hypoglycaemia triggers glucagon secretion, which restores normal plasma glucose levels by stimulation of hepatic glucose production. This counterregulatory mechanism is impaired in diabetes. Here we show in mice that therapeutic concentrations of insulin inhibit glucagon secretion by an indirect (paracrine) mechanism mediated by stimulation of intra-islet somatostatin release. Insulin's capacity to inhibit glucagon secretion is lost following genetic ablation of insulin receptors in the somatostatin-secreting δ-cells, when insulin-induced somatostatin secretion is suppressed by dapagliflozin (an inhibitor of sodium-glucose co-tranporter-2; SGLT2) or when the action of secreted somatostatin is prevented by somatostatin receptor (SSTR) antagonists. Administration of these compounds in vivo antagonises insulin's hypoglycaemic effect. We extend these data to isolated human islets. We propose that SSTR or SGLT2 antagonists should be considered as adjuncts to insulin in diabetes therapy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30635569 · DOI · PMC6329806
Mutant huntingtin expression in somatostatin-positive interneurons contributes to neurophysiological and behavioral phenotypes in BACHD mice [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Huntington's disease (HD) is caused by expansion of the polyglutamine stretch in the widely expressed huntingtin (HTT) protein.
- Closing excerpt
- Additionally, expression of mHTT in striatal SST-INs cell autonomously drives their increased excitability.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (179 words)
Huntington's disease (HD) is caused by expansion of the polyglutamine stretch in the widely expressed huntingtin (HTT) protein. Patients with HD have motor, psychiatric and cognitive changes due to changes in a variety of neural circuits. Somatostatin-expressing interneurons (SST-INs) can regulate neural circuits largely by inhibiting their target cells. Behaviorally, brain-wide inhibition of SST-INs increased anxiety in mice. Silencing striatal SST-INs caused a decrease in movement in the open field. Mutant HTT (mHTT)-expressing mice exhibited abnormal motor, cognitive and psychiatric-like changes, as well as electrophysiological changes in a variety of neurons, including striatal SST-INs. However, it is unknown whether cell-autonomous expression of mHTT in SST-INs contributes to HD-associated behavioral phenotypes or causes abnormal electrophysiological changes in striatal SST-INs. To address these questions, we reduced mHTT expression in SST-INs throughout the brain of BACHD mice. Our findings show that brain-wide reduction of mHTT in SST-INs rescues anxiety-like behavior in male BACHD mice in the light-dark box, without improving performance in the open field or on the rotarod. Additionally, expression of mHTT in striatal SST-INs cell autonomously drives their increased excitability.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41648922 · DOI · PMC13054931
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article A Consensus Statement on acromegaly therapeutic outcomes [5]
- Research article Somatostatin-expressing neurons in cortical networks [6]
- Research article Multidisciplinary management of acromegaly: A consensus [7]
- Research article Review article: somatostatin analogues in the treatment of gastroenteropancreatic neuroendocrine (carcinoid) tumours [8]
- Research article Meta-analysis: vasoactive medications for the management of acute variceal bleeds [9]
- Research article Somatostatin receptor ligands and resistance to treatment in pituitary adenomas [10]
References
- Gomes-Porras M, Cárdenas-Salas J, Álvarez-Escolá C. Somatostatin Analogs in Clinical Practice: a Review. . 2020. PMID 32121432 · DOI · PMC7084228
- Stueven AK, Kayser A, Wetz C, Amthauer H, Wree A, Tacke F, et al.. Somatostatin Analogues in the Treatment of Neuroendocrine Tumors: Past, Present and Future. . 2019. PMID 31234481 · DOI · PMC6627451
- Vergari E, Knudsen JG, Ramracheya R, Salehi A, Zhang Q, Adam J, et al.. Insulin inhibits glucagon release by SGLT2-induced stimulation of somatostatin secretion. . 2019. PMID 30635569 · DOI · PMC6329806
- Fowler JA, Scarduzio M, Pool C, Mahan CD, Gray M. Mutant huntingtin expression in somatostatin-positive interneurons contributes to neurophysiological and behavioral phenotypes in BACHD mice. . 2026. PMID 41648922 · DOI · PMC13054931
- Melmed S, Bronstein MD, Chanson P, Klibanski A, Casanueva FF, Wass JAH, et al.. A Consensus Statement on acromegaly therapeutic outcomes. Nat Rev Endocrinol. 2018. PMID 30050156 · DOI · PMC7136157
- Urban-Ciecko J, Barth AL. Somatostatin-expressing neurons in cortical networks. Nat Rev Neurosci. 2016. PMID 27225074 · DOI · PMC5635659
- Giustina A, Barkhoudarian G, Beckers A, Ben-Shlomo A, Biermasz N, Biller B, et al.. Multidisciplinary management of acromegaly: A consensus. Rev Endocr Metab Disord. 2020. PMID 32914330 · DOI · PMC7942783
- Modlin IM, Pavel M, Kidd M, Gustafsson BI. Review article: somatostatin analogues in the treatment of gastroenteropancreatic neuroendocrine (carcinoid) tumours. Aliment Pharmacol Ther. 2010. PMID 19845567 · DOI
- Wells M, Chande N, Adams P, Beaton M, Levstik M, Boyce E, et al.. Meta-analysis: vasoactive medications for the management of acute variceal bleeds. Aliment Pharmacol Ther. 2012. PMID 22486630 · DOI
- Cuevas-Ramos D, Fleseriu M. Somatostatin receptor ligands and resistance to treatment in pituitary adenomas. J Mol Endocrinol. 2014. PMID 24647046 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.