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 (727 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 12-kDa cysteine-rich polypeptide hormone secreted by fat cells in the adipose tissue. It is the founding member of the resistin-like molecule (RELM) hormone family. Resistin suppresses the ability of insulin to stimulate cellular glucose uptake.
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: Adipocyte Cysteine-Rich Secreted Protein FIZZ3; Adipocyte Cysteine Rich Secreted Protein FIZZ3.
Where it fits in the MeSH classification
- Broader topics
- Adipokines
Related concepts
- Fat Cells
- Adipose Tissue
- Insulin
- Glucose
Research landscape
PubMed indexes 2,875 records tagged with the MeSH heading “Resistin” (counts retrieved 2026-10-31). 567 of them (19.7%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 1,400 records.
Reviews account for 306 records (10.6%) and meta-analyses for 52. Randomized controlled trials number 104 (3.6%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 950 |
| 2010-2019 | 1,400 |
| 2020 onward | 567 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 306 | 10.6% |
| Meta-analyses | 52 | 1.8% |
| Randomized controlled trials | 104 | 3.6% |
Method: PubMed query "Resistin"[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 |
|---|---|---|---|---|
| Resistin, a Novel Host Defense Peptide of Innate Immunity | 2021 | Review article Design not recorded in structured metadata | 82 | cc by PMID 34220862 · DOI · PMC8253364 |
| An Overview of the Role of Adipokines in Cardiometabolic Diseases | 2020 | Review article Design not recorded in structured metadata | 80 | cc by PMID 33182462 · DOI · PMC7665135 |
| High insulin and leptin increase resistin and inflammatory cytokine production from human mononuclear cells | 2013 | Clinical trial Design not recorded in structured metadata | 74 | cc by PMID 23484124 · DOI · PMC3591160 |
| Exosome-Mediated Lectin Pathway and Resistin-MIF-AA Metabolism Axis Drive Immune Dysfunction in Immune Thrombocytopenia | 2025 | Research article Design not recorded in structured metadata | 14 | cc by PMID 39792656 · DOI · PMC11905005 |
Resistin, a Novel Host Defense Peptide of Innate Immunity [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Resistin, a cysteine-rich protein, expressed in adipocytes, was initially proposed as a link between obesity and diabetes in mice.
- Closing excerpt
- The review aims to summarize current knowledge about the biological properties, functions, and related mechanisms of resistin in host defense, which provides new insights into the pleiotropic biological function of resistin and yields promising strategies for developing new antimicrobial therapeutic agents.
- 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 (135 words)
Resistin, a cysteine-rich protein, expressed in adipocytes, was initially proposed as a link between obesity and diabetes in mice. In humans, resistin is considered to be a pro-inflammatory molecule expressed in immune cells, which plays a regulatory role in many chronic inflammatory diseases, metabolic diseases, infectious diseases, and cancers. However, increasing evidence shows that resistin functions as a host defense peptide of innate immunity, in terms of its wide-spectrum anti-microbial activity, modulation of immunity, and limitation of microbial product-induced inflammation. To date, the understanding of resistin participating in host defense mechanism is still limited. The review aims to summarize current knowledge about the biological properties, functions, and related mechanisms of resistin in host defense, which provides new insights into the pleiotropic biological function of resistin and yields promising strategies for developing new antimicrobial therapeutic agents.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34220862 · DOI · PMC8253364
An Overview of the Role of Adipokines in Cardiometabolic Diseases [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Obesity as an independent risk factor for cardiovascular diseases (CVDs) leads to an increase in morbidity, mortality, and a shortening of life span.
- Closing excerpt
- However, more studies should be designed to clarify the association between obesity, adipokine changes, and the occurrence of CVDs.
- 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 (177 words)
Obesity as an independent risk factor for cardiovascular diseases (CVDs) leads to an increase in morbidity, mortality, and a shortening of life span. The changes in heart structure and function as well as metabolic profile are caused by obese people, including those free of metabolic disorders. Obesity alters heart function structure and affects lipid and glucose metabolism, blood pressure, and increase inflammatory cytokines. Adipokines, specific cytokines of adipocytes, are involved in the progression of obesity and the associated co-morbidities. In the current study, we review the scientific evidence on the effects of obesity on CVDs, focusing on the changes in adipokines. Several adipokines have anti-inflammatory and cardioprotective effects comprising omentin, apelin, adiponectin, and secreted frizzled-related protein (Sfrp-5). Other adipokines have pro-inflammatory impacts on the cardiovascular system and obesity including leptin, tumor necrosis factor (TNF), retinol-binding protein4 (RBP-4), visfatin, resistin, and osteopontin. We found that obesity is associated with multiple CVDs, but can only occur in unhealthy metabolic patients. However, more studies should be designed to clarify the association between obesity, adipokine changes, and the occurrence of CVDs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33182462 · DOI · PMC7665135
High insulin and leptin increase resistin and inflammatory cytokine production from human mononuclear cells [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Resistin and the proinflammatory cytokines, such as TNF- α , IL-6, and IL-1 β , produced by adipocytes, and macrophages, are considered to be important modulators of chronic inflammation contributing to the development of obesity and atherosclerosis.
- Closing excerpt
- Therefore, the above increased production may contribute to detrimental effects of their increased adipocyte-derived circulating levels on systemic inflammation, insulin sensitivity, and endothelial function of these patients.
- 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 (215 words)
Resistin and the proinflammatory cytokines, such as TNF- α , IL-6, and IL-1 β , produced by adipocytes, and macrophages, are considered to be important modulators of chronic inflammation contributing to the development of obesity and atherosclerosis. Human monocyte-enriched mononuclear cells, from ten healthy individuals, were exposed to high concentrations of insulin, leptin, and glucose (alone or in combination) for 24 hours in vitro. Resistin, TNF- α , IL-6, and IL-1 β production was examined and compared to that in untreated cells. High insulin and leptin concentrations significantly upregulated resistin and the cytokines. The subsequent addition of high glucose significantly upregulated resistin and TNF- α mRNA and protein secretion, while it did not have any effect on IL-6 or IL-1 β production. By comparison, exposure to dexamethasone reduced TNF- α , IL-6, and IL-1 β production, while at this time point it increased resistin protein secretion. These data suggest that the expression of resistin, TNF- α , IL-6, and IL-1 β from human mononuclear cells, might be enhanced by the hyperinsulinemia and hyperleptinemia and possibly by the hyperglycemia in metabolic diseases as obesity, type 2 diabetes, and atherosclerosis. Therefore, the above increased production may contribute to detrimental effects of their increased adipocyte-derived circulating levels on systemic inflammation, insulin sensitivity, and endothelial function of these patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 23484124 · DOI · PMC3591160
Exosome-Mediated Lectin Pathway and Resistin-MIF-AA Metabolism Axis Drive Immune Dysfunction in Immune Thrombocytopenia [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by reduced platelet levels and heightened susceptibility to bleeding resulting from augmented autologous platelet destruction and diminished thrombopoiesis.
- Closing excerpt
- Taken together, the findings indicate that the lectin pathway of the complement system, resistin, MIF, and AA metabolism may serve as promising targets for ITP treatment, offering novel perspectives on potential therapeutic interventions.
- 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 (200 words)
Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by reduced platelet levels and heightened susceptibility to bleeding resulting from augmented autologous platelet destruction and diminished thrombopoiesis. Although antibody-mediated autoimmune reactions are widely recognized as primary factors, the precise etiological agents that trigger ITP remain unidentified. The pathogenesis of ITP remains unclear owing to the absence of comprehensive high-throughput data, except for the belated emergence of autoreactive antibodies. In this study, using flow cytometry (FCM), proteomics, and single-cell RNA sequencing of samples from patients with ITP, it is shown that exosome-mediated lectin complement pathway is involved in the pathogenesis of ITP, which triggers and enlarges the complement activation cascade without effective regulation because of downregulated CD55. The activated complement system enhances the immune response and resistin and further Macrophage Migration Inhibitory Factor (MIF) triggers several proinflammatory signaling pathways, which contribute to the survival of hyperactivated immune cells and dysfunctional arachidonic acid (AA) metabolism. The resistin and MIF are also identified as potential contributors to resistance to glucocorticoid therapy. Taken together, the findings indicate that the lectin pathway of the complement system, resistin, MIF, and AA metabolism may serve as promising targets for ITP treatment, offering novel perspectives on potential therapeutic interventions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39792656 · DOI · PMC11905005
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 Resistin: functional roles and therapeutic considerations for cardiovascular disease [5]
- Research article The role of resistin as a regulator of inflammation: Implications for various human pathologies [6]
- Research article Adipocytokines: leptin--the classical, resistin--the controversical, adiponectin--the promising, and more to come [7]
- Research article Human resistin: found in translation from mouse to man [8]
- Research article Adipokines: implications for female fertility and obesity [9]
- Research article Resistin in metabolism, inflammation, and disease [10]
References
- Li Y, Yang Q, Cai D, Guo H, Fang J, Cui H, et al.. Resistin, a Novel Host Defense Peptide of Innate Immunity. . 2021. PMID 34220862 · DOI · PMC8253364
- Farkhondeh T, Llorens S, Pourbagher-Shahri AM, Ashrafizadeh M, Talebi M, Shakibaei M, et al.. An Overview of the Role of Adipokines in Cardiometabolic Diseases. . 2020. PMID 33182462 · DOI · PMC7665135
- Tsiotra PC, Boutati E, Dimitriadis G, Raptis SA. High insulin and leptin increase resistin and inflammatory cytokine production from human mononuclear cells. . 2013. PMID 23484124 · DOI · PMC3591160
- Li J, Wang X, Chen Y, Sun X, Fu L, Xin Q, et al.. Exosome-Mediated Lectin Pathway and Resistin-MIF-AA Metabolism Axis Drive Immune Dysfunction in Immune Thrombocytopenia. . 2025. PMID 39792656 · DOI · PMC11905005
- Jamaluddin MS, Weakley SM, Yao Q, Chen C. Resistin: functional roles and therapeutic considerations for cardiovascular disease. Br J Pharmacol. 2012. PMID 21545576 · DOI · PMC3315035
- Filková M, Haluzík M, Gay S, Senolt L. The role of resistin as a regulator of inflammation: Implications for various human pathologies. Clin Immunol. 2009. PMID 19740705 · DOI
- Koerner A, Kratzsch J, Kiess W. Adipocytokines: leptin--the classical, resistin--the controversical, adiponectin--the promising, and more to come. Best Pract Res Clin Endocrinol Metab. 2005. PMID 16311215 · DOI
- Schwartz DR, Lazar MA. Human resistin: found in translation from mouse to man. Trends Endocrinol Metab. 2011. PMID 21497511 · DOI · PMC3130099
- Mitchell M, Armstrong DT, Robker RL, Norman RJ. Adipokines: implications for female fertility and obesity. Reproduction. 2005. PMID 16264089 · DOI
- Tripathi D, Kant S, Pandey S, Ehtesham NZ. Resistin in metabolism, inflammation, and disease. FEBS J. 2020. PMID 32255270 · 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.