ArticleJournal of lipid research2009
Serum amyloid A3 does not contribute to circulating SAA levels.
Article in Journal of lipid research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.
- Association between serum amyloid A levels and coronary heart disease: a systematic review and meta-analysis of 26 studies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Pooled it
- Association between serum amyloid A and obesity: a meta-analysis and systematic review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2010Pooled it
- Cold-induced serum amyloid A3 amplifies cAMP-PKA signaling to drive adaptive thermogenesis in brown adipocytes.Journal of physiology and biochemistry · 2026Article
- Podoplanin-positive cell-derived small extracellular vesicles contribute to cardiac amyloidosis after myocardial infarction.Cell reports · 2025Article
- Serum amyloid A and metabolic disease: evidence for a critical role in chronic inflammatory conditions.Frontiers in cardiovascular medicine · 2023Review
- Non-alcoholic fatty liver disease and liver secretome.Archives of pharmacal research · 2022Review
- Comparison between genetic and pharmaceutical disruption of Ldlr expression for the development of atherosclerosis.Journal of lipid research · 2022Article
- The Influence of Obesity and Weight Loss on the Bioregulation of Innate/Inflammatory Responses: Macrophages and Immunometabolism.Nutrients · 2022Review
- Article
- Role of Serum Amyloid A in Abdominal Aortic Aneurysm and Related Cardiovascular Diseases.Biomolecules · 2021Review
- Sexually Dimorphic Relationships Among Saa3 (Serum Amyloid A3), Inflammation, and Cholesterol Metabolism Modulate Atherosclerosis in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Induction of Serum Amyloid A3 in Mouse Mammary Epithelial Cells Stimulated with Lipopolysaccharide and Lipoteichoic Acid.Animals : an open access journal from MDPI · 2021Article
- Identification ofAging · 2020Article
- Serum amyloid A-containing HDL binds adipocyte-derived versican and macrophage-derived biglycan, reducing its antiinflammatory properties.JCI insight · 2020Article
- Biological Characterization of Commercial Recombinantly Expressed Immunomodulating Proteins Contaminated with Bacterial Products in the Year 2020: The SAA3 Case.Mediators of inflammation · 2020Article
- Beyond adiponectin and leptin: adipose tissue-derived mediators of inter-organ communication.Journal of lipid research · 2019Review
- Article
- Serum amyloid A predisposes inflammatory tumor microenvironment in triple negative breast cancer.Oncotarget · 2019Article
- Article
- Continuous PTH in Male Mice Causes Bone Loss Because It Induces Serum Amyloid A.Endocrinology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Adipose tissue secretes proteins like serum amyloid A (SAA), which plays important roles in local and systemic inflammation. Circulating SAA levels increase in obese humans, but the roles of adipose-derived SAA and hyperlipidemia in this process are unclear. We took advantage of the difference in the inducible isoforms of SAA secreted by adipose tissue (SAA3) and liver (SAA1 and 2) of mice to evaluate whether adipose tissue contributes to the circulating pool of SAA in obesity and hyperlipidemia. Genetically obese (ob/ob) mice, but not hyperlipidemic mice deficient in apolipoprotein E (Apoe(-/-)), had significantly higher circulating levels of SAA than their littermate controls. SAA1/2 mRNA expression in the liver and SAA3 mRNA expression in intra-abdominal fat were significantly higher in obese than thin mice, but they were not affected by hyperlipidemia in Apoe(-/-) mice. However, only SAA1/2 and the constitutive form of SAA (SAA4) could be detected in the circulation by mass spectrometric analysis of HDL, the major carrier of circulating SAA. In contrast, SAA3 could be detected in medium from cultured adipocytes. Our findings indicate that the expression of SAA3 in adipose tissue is upregulated by obesity, but it does not contribute to the circulating pool of SAA in mice.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.