ArticleNature communications2022
Loss of immunity-related GTPase GM4951 leads to nonalcoholic fatty liver disease without obesity.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Structural insights into GM4951 as a lipid droplet GTPase regulating hepatic lipid metabolism.Nature communications · 2025Article
- Preventing effect of plant extracts and omega-3 on age-related cognitive decline in male mice.Brain, behavior, & immunity - health · 2025Article
- A hypomorphic Mpi mutation unlocks an in vivo tool for studying global N-glycosylation deficiency.JCI insight · 2025Article
- KBTBD2 controls bone development by regulating IGF-1 signaling during osteoblast differentiation.Cell death and differentiation · 2025Article
- Transcriptomic Signatures of the Foetal Liver and Late Prenatal Development in Vitrified Rabbit Embryos.Veterinary sciences · 2024Article
- Exploring the role of genetic variations in NAFLD: implications for disease pathogenesis and precision medicine approaches.European journal of medical research · 2024Review
- Article
- Transcriptomics-based anti-tuberculous mechanism of traditional Chinese polyherbal preparation NiuBeiXiaoHe intermediates.Frontiers in pharmacology · 2024Article
- Correlation between nonalcoholic fatty liver disease and left ventricular diastolic dysfunction in non-obese adults: a cross-sectional study.BMC gastroenterology · 2023Article
- Metabolic effects of CCL5 deficiency in lean and obese mice.Frontiers in immunology · 2022Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Obesity and diabetes are well known risk factors for nonalcoholic fatty liver disease (NAFLD), but the genetic factors contributing to the development of NAFLD remain poorly understood. Here we describe two semi-dominant allelic missense mutations (Oily and Carboniferous) of Predicted gene 4951 (Gm4951) identified from a forward genetic screen in mice. GM4951 deficient mice developed NAFLD on high fat diet (HFD) with no changes in body weight or glucose metabolism. Moreover, HFD caused a reduction in the level of Gm4951, which in turn promoted the development of NAFLD. Predominantly expressed in hepatocytes, GM4951 was verified as an interferon inducible GTPase. The NAFLD in Gm4951 knockout mice was associated with decreased lipid oxidation in the liver and no defect in hepatic lipid secretion. After lipid loading, hepatocyte GM4951 translocated to lipid droplets (LDs), bringing with it hydroxysteroid 17β-dehydrogenase 13 (HSD17B13), which in the absence of GM4951 did not undergo this translocation. We identified a rare non-obese mouse model of NAFLD caused by GM4951 deficiency and define a critical role for GTPase-mediated translocation in hepatic lipid metabolism.
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