ArticleMolecular metabolism2018
Adipose specific disruption of seipin causes early-onset generalised lipodystrophy and altered fuel utilisation without severe metabolic disease.
Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- Metabolic-Associated Steatotic Liver Disease and FGF21 Dysregulation in Seipin-Deficient andInternational journal of molecular sciences · 2025Article
- Experimental analysis of bone marrow adipose tissue and bone marrow adipocytes: An update from the bone marrow adiposity society (BMAS).Bone reports · 2025Review
- Hydroxysteroid 17β-dehydrogenase 13 (Hsd17b13) knockdown attenuates liver steatosis in high-fat diet obese mice.Experimental physiology · 2025Article
- Preclinical evaluation of tissue-selective gene therapies for congenital generalised lipodystrophy.Gene therapy · 2024Article
- DIDO is necessary for the adipogenesis that promotes diet-induced obesity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- GLP-1 receptor agonist improves metabolic disease in a pre-clinical model of lipodystrophy.Frontiers in endocrinology · 2024Article
- Gene therapy restores adipose tissue and metabolic health in a pre-clinical mouse model of lipodystrophy.Molecular therapy. Methods & clinical development · 2022Article
- Reduced phosphatidylcholine synthesis suppresses the embryonic lethality of seipin deficiency.Life metabolism · 2022Article
- Lipolysis of bone marrow adipocytes is required to fuel bone and the marrow niche during energy deficits.eLife · 2022Article
- Role of Seipin in Human Diseases and Experimental Animal Models.Biomolecules · 2022Review
- Seipin Deficiency as a Model of Severe Adipocyte Dysfunction: Lessons from Rodent Models and Teaching for Human Disease.International journal of molecular sciences · 2022Review
- Not Enough Fat: Mouse Models of Inherited Lipodystrophy.Frontiers in endocrinology · 2022Review
- Seipin: harvesting fat and keeping adipocytes healthy.Trends in cell biology · 2021Review
- Preclinical models for investigating how bone marrow adipocytes influence bone and hematopoietic cellularity.Best practice & research. Clinical endocrinology & metabolism · 2021Review
- Phosphoprotein enriched in astrocytes (PEA)-15 is a novel regulator of adipose tissue expansion.Scientific reports · 2021Article
- Ablation ofJBMR plus · 2021Article
- Article
- Exercise Increases Bone in SEIPIN Deficient Lipodystrophy, Despite Low Marrow Adiposity.Frontiers in endocrinology · 2021Article
- Protein Arginine Methyltransferase PRMT5 Regulates Fatty Acid Metabolism and Lipid Droplet Biogenesis in White Adipose Tissues.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Myeloma Cells Down-Regulate Adiponectin in Bone Marrow Adipocytes Via TNF-Alpha.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
objectiveMutations to the BSCL2 gene disrupt the protein seipin and cause the most severe form of congenital generalised lipodystrophy (CGL). Affected individuals exhibit a near complete loss of white adipose tissue (WAT) and suffer from metabolic disease. Seipin is critical for adipocyte development in culture and mice with germline disruption to Bscl2 recapitulate the effects of BSCL2 disruption in humans. Here we examined whether loss of Bscl2 specifically in developing adipocytes in vivo is sufficient to prevent adipose tissue development and cause all features observed with congenital BSCL2 disruption.
methodsWe generated and characterised a novel mouse model of Bscl2 deficiency in developing adipocytes (Ad-B2
resultsWe demonstrate that Ad-B2
conclusionsOur findings demonstrate that disruption of Bscl2 specifically in developing adipocytes is sufficient to cause the early-onset generalised lipodystrophy observed in patients with mutations in BSCL2. However, this significant reduction in adipose mass does not cause the overt metabolic dysfunction seen in Bscl2 knockout mice, even following a high-fat diet challenge.
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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.