ArticleScientific reports2016
Factor XIII-A transglutaminase deficient mice show signs of metabolically healthy obesity on high fat diet.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Fibrin formation and lysis in hyperglycaemia - molecular and cellular drivers.Current opinion in hematology · 2026Review
- Integrative Transcriptomics and Machine Learning Identify Macrophage-Associated Biomarkers in Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2026Article
- F13A1-Mediated Macrophage Activation Promotes MASH Progression via the PKM2/HIF1A Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Transcriptomic suppression of immune and ECM stability in skeletal muscle of patients with chronic kidney disease.PloS one · 2026Article
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- Intermittent Cold Exposure Induces Distinct Proteomic Signatures in White Adipose Tissue of Mice.International journal of molecular sciences · 2025Article
- Circulating plasma fibronectin affects tissue insulin sensitivity, adipocyte differentiation, and transcriptional landscape of adipose tissue in mice.Physiological reports · 2024Article
- Collagens Regulating Adipose Tissue Formation and Functions.Biomedicines · 2023Review
- Elimination of fibrin polymer formation or crosslinking, but not fibrinogen deficiency, is protective against diet-induced obesity and associated pathologies.Journal of thrombosis and haemostasis : JTH · 2022Article
- Genome Profiling of H3k4me3 Histone Modification in Human Adipose Tissue during Obesity and Insulin Resistance.Biomedicines · 2021Article
- F13A1 transglutaminase expression in human adipose tissue increases in acquired excess weight and associates with inflammatory status of adipocytes.International journal of obesity (2005) · 2021Article
- Factor XIII-A in Diseases: Role Beyond Blood Coagulation.International journal of molecular sciences · 2021Review
- Transglutaminases and Obesity in Humans: Association ofInternational journal of molecular sciences · 2020Article
- Fibroblast activation protein restrains adipogenic differentiation and regulates matrix-mediated mTOR signaling.Matrix biology : journal of the International Society for Matrix Biology · 2019Article
- Transglutaminases in Monocytes and Macrophages.Medical sciences (Basel, Switzerland) · 2018Review
- Thrombin promotes diet-induced obesity through fibrin-driven inflammation.The Journal of clinical investigation · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
F13A1 gene, which encodes for Factor XIII-A blood clotting factor and a transglutaminase enzyme, was recently identified as a potential causative gene for obesity in humans. In our previous in vitro work, we showed that FXIII-A regulates preadipocyte differentiation and modulates insulin signaling via promoting plasma fibronectin assembly into the extracellular matrix. To understand the role of FXIII-A in whole body energy metabolism, here we have characterized the metabolic phenotype of F13a1-/- mice. F13a1-/- and F13a1+/+ type mice were fed chow or obesogenic, high fat diet for 20 weeks. Weight gain, total fat mass and fat pad mass, glucose handling, insulin sensitivity, energy expenditure and, morphological and biochemical analysis of adipose tissue was performed. We show that mice lacking FXIII-A gain weight on obesogenic diet, similarly as wild type mice, but exhibit a number of features of metabolically healthy obesity such as protection from developing diet-induced insulin resistance and hyperinsulinemia. Mice also show normal fasting glucose levels, larger adipocytes, decreased extracellular matrix accumulation and inflammation of adipose tissue, as well as decreased circulating triglycerides. This study reveals that FXIII-A transglutaminase can regulate whole body insulin sensitivity and may have a role in the development of diet-induced metabolic disturbances.
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