ArticleGene2013
The C57BL/6J Niemann-Pick C1 mouse model with decreased gene dosage has impaired glucose tolerance independent of body weight.
Article in Gene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Organ Weights inInternational journal of molecular sciences · 2022Article
- Understanding and Treating Niemann-Pick Type C Disease: Models Matter.International journal of molecular sciences · 2020Review
- Current Challenges in Understanding the Cellular and Molecular Mechanisms in Niemann-Pick Disease Type C1.International journal of molecular sciences · 2019Review
- Associations of Mitochondrial and Nuclear Mitochondrial Variants and Genes with Seven Metabolic Traits.American journal of human genetics · 2019Article
- The Extending Spectrum of NPC1-Related Human Disorders: From Niemann-Pick C1 Disease to Obesity.Endocrine reviews · 2018Review
- Evaluation of Two Liver Treatment Strategies in a Mouse Model of Niemann-Pick-Disease Type C1.International journal of molecular sciences · 2018Article
- Exacerbating and reversing lysosomal storage diseases: from yeast to humans.Microbial cell (Graz, Austria) · 2017Review
- Neurological Dysfunction in Early Maturity of a Model for Niemann-Pick C1 Carrier Status.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016Article
- Article
- Lipotoxicity in the pancreatic beta cell: not just survival and function, but proliferation as well?Current diabetes reports · 2014Review
- Article
- Differential Association of Niemann-Pick C1 Gene Polymorphisms with Maternal Prepregnancy Overweight and Gestational Diabetes.Journal of diabetes and obesityArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The human Niemann-Pick C1 (NPC1) gene has been found to be associated with extreme (early-onset and morbid-adult) obesity and type 2 diabetes independent of body weight. We previously performed growth studies using BALB/cJ Npc1 normal (Npc1+/+) and Npc1 heterozygous (Npc1+/-) mice and determined that decreased Npc1 gene dosage interacts with a high-fat diet to promote weight gain and adiposity. The present study was performed using both BALB/cJ and C57BL/6J Npc1+/+ and Npc1+/- mice to determine if decreased Npc1 gene dosage predisposes to metabolic features associated with type 2 diabetes. The results indicated that C57BL/6J Npc1+/- mice, but not BALB/cJ Npc1+/- mice, have impaired glucose tolerance when fed a low-fat diet and independent of body weight. The results also suggest that an accumulation of liver free fatty acids and hepatic lipotoxicity marked by an elevation in the amount of plasma alanine aminotransferase (ALT) may be responsible for hepatic insulin resistance and impaired glucose tolerance. Finally, the peroxisome-proliferator activated receptor α (PPARα) and sterol regulatory element-binding protein-1 (SREBP-1) pathways known to have a central role in regulating free fatty acid metabolism were downregulated in the livers, but not in the adipose or muscle, of C57BL/6J Npc1+/- mice compared to C57BL/6J Npc1+/+ mice. Therefore, decreased Npc1 gene dosage among two different mouse strains interacts with undefined modifying genes to manifest disparate yet often related metabolic diseases.
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Registered trials
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