ArticlePloS one2015
Lack of the Lysosomal Membrane Protein, GLMP, in Mice Results in Metabolic Dysregulation in Liver.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Convergent subgenome dominance but with lineage-specific functional divergence of homoeologs during cave adaptation: insights from full-length transcriptomes of Sinocyclocheilus species.Frontiers in zoology · 2025Article
- Fas apoptotic inhibitor molecule 2 mitigates metabolic dysfunction-associated fatty liver disease through autophagic CRTC2 degradation.Experimental & molecular medicine · 2025Article
- Essential role of MFSD1-GLMP-GIMAP5 in lymphocyte survival and liver homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
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- Common Transcriptional Program of Liver Fibrosis in Mouse Genetic Models and Humans.International journal of molecular sciences · 2021Article
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- Cortical atrophy and hypofibrinogenemia due to FGG and TBCD mutations in a single family: a case report.BMC medical genetics · 2018Article
- Age-dependent development of liver fibrosis in Glmp (gt/gt) mice.Fibrogenesis & tissue repair · 2016Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ablation of glycosylated lysosomal membrane protein (GLMP, formerly known as NCU-G1) has been shown to cause chronic liver injury which progresses into liver fibrosis in mice. Both lysosomal dysfunction and chronic liver injury can cause metabolic dysregulation. Glmp gt/gt mice (formerly known as Ncu-g1gt/gt mice) were studied between 3 weeks and 9 months of age. Body weight gain and feed efficiency of Glmp gt/gt mice were comparable to wild type siblings, only at the age of 9 months the Glmp gt/gt siblings had significantly reduced body weight. Reduced size of epididymal fat pads was accompanied by hepatosplenomegaly in Glmp gt/gt mice. Blood analysis revealed reduced levels of blood glucose, circulating triacylglycerol and non-esterified fatty acids in Glmp gt/gt mice. Increased flux of glucose, increased de novo lipogenesis and lipid accumulation were detected in Glmp gt/gt primary hepatocytes, as well as elevated triacylglycerol levels in Glmp gt/gt liver homogenates, compared to hepatocytes and liver from wild type mice. Gene expression analysis showed an increased expression of genes involved in fatty acid uptake and lipogenesis in Glmp gt/gt liver compared to wild type. Our findings are in agreement with the metabolic alterations observed in other mouse models lacking lysosomal proteins, and with alterations characteristic for advanced chronic liver injury.
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Registered trials
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