ArticleObesity (Silver Spring, Md.)2011
Follistatin and follistatin like-3 differentially regulate adiposity and glucose homeostasis.
Article in Obesity (Silver Spring, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- Alterations in systemic and skeletal muscle myostatin regulation are most prominent at disease onset and associate with muscle-related outcomes in idiopathic inflammatory myopathies.Arthritis research & therapy · 2026Article
- Association Between Maternal Gestational Diabetes, Cord Blood DNA Methylation, and Offspring Neurodevelopment.International journal of molecular sciences · 2026Article
- Crosstalk Between Skeletal Muscle and Proximal Connective Tissues in Lipid Dysregulation in Obesity and Type 2 Diabetes.Metabolites · 2025Review
- Activin Actions in Adipocytes.The Journal of clinical endocrinology and metabolism · 2025Review
- Activin B improves glucose metabolism via induction of Fgf21 and hepatic glucagon resistance.Nature communications · 2025Article
- Review
- Myostatin and Activin A as Biomarkers of Sarcopenia in Inflammatory Bowel Disease Patients.Nutrients · 2024Article
- FSTL3 promotes tumor immune evasion and attenuates response to anti-PD1 therapy by stabilizing c-Myc in colorectal cancer.Cell death & disease · 2024Article
- Review
- Disentangling the aetiological pathways between body mass index and site-specific cancer risk using tissue-partitioned Mendelian randomisation.British journal of cancer · 2023Article
- FSTL3 is highly expressed in adipose tissue of individuals with overweight or obesity and is associated with inflammation.Obesity (Silver Spring, Md.) · 2023Article
- Metabolic and proteomic signatures of type 2 diabetes subtypes in an Arab population.Nature communications · 2022Article
- Can Exercise Training Alter Human Skeletal Muscle DNA Methylation?Metabolites · 2022Article
- Follistatin-Like Proteins: Structure, Functions and Biomedical Importance.Biomedicines · 2021Review
- TGF-β Signaling in Pancreatic Islet β Cell Development and Function.Endocrinology · 2021Review
- Novel Roles of Follistatin/Myostatin in Transforming Growth Factor-β Signaling and Adipose Browning: Potential for Therapeutic Intervention in Obesity Related Metabolic Disorders.Frontiers in endocrinology · 2021Review
- Targeted Analysis of Three Hormonal Systems Identifies Molecules Associated with the Presence and Severity of NAFLD.The Journal of clinical endocrinology and metabolism · 2020Observational
- Beyond the bone: Bone morphogenetic protein signaling in adipose tissue.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2019Review
- Profiling Cellular Processes in Adipose Tissue during Weight Loss Using Time Series Gene Expression.Genes · 2018Article
- Early second trimester maternal serum markers in the prediction of gestational diabetes mellitus.Journal of diabetes investigation · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Transforming growth factor-β superfamily ligands, including activin and myostatin, modulate body composition, islet function, and glucose homeostasis. Their bioactivity is controlled by the antagonists follistatin (FST) and FST like-3 (FSTL3). The hypothesis tested was that FST and FSTL3 have distinct roles in regulating body composition, glucose homeostasis, and islet function through regulation of activin and myostatin bioactivity. Three genetic mutant mouse lines were created. FSTL3 knockout (FSTL3 KO), a mouse line producing only the FST288 isoform (FST288-only) and a double mutant (2xM) in which the lines were crossed. FST288-only males were lighter that wild-type (WT) littermates while FSTL3 KO and 2xM males had reduced perigonadal fat pad weights. However, only 2xM mice had increased whole body fat mass and decreased lean mass by quantitative nuclear magnetic resonance (qNMR). Fasting glucose levels in FSTL3 WT and KO mice were lower than FST mice in younger animals but were higher in older mice. Serum insulin and pancreatic insulin content in 2xM mice was significantly elevated over other genotypes. Nevertheless, 2xM mice were relatively insulin resistant and glucose intolerant compared to FST288-only and WT mice. Fractional islet area and proportion of β-cells/islet were increased in FSTL3 KO and 2xM, but not FST288-only mice. Despite their larger size, islets from FSTL3 KO and 2xM mice were not functionally enhanced compared to WT mice. These results demonstrate that body composition and glucose homeostasis are differentially regulated by FST and FSTL3 and that their combined loss is associated with increased fat mass and insulin resistance despite elevated insulin production.
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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.