ArticleProceedings of the National Academy of Sciences of the United States of America2015
Replacing SNAP-25b with SNAP-25a expression results in metabolic disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Integrated Ultrasound Characterization of the Diet-Induced Obesity (DIO) Model in Young Adult c57bl/6j Mice: Assessment of Cardiovascular, Renal and Hepatic Changes.Journal of imaging · 2024Article
- Western diet-induced ultrastructural changes in mouse pancreatic acinar cells.Frontiers in cell and developmental biology · 2024Article
- Article
- SNAP25 mutation disrupts metabolic homeostasis, steroid hormone production and central neurobehavior.Biochimica et biophysica acta. Molecular basis of disease · 2022Article
- Disorganization and degeneration of liver sympathetic innervations in nonalcoholic fatty liver disease revealed by 3D imaging.Science advances · 2021Article
- Regulatory roles and mechanisms of alternative RNA splicing in adipogenesis and human metabolic health.Cell & bioscience · 2021Review
- Upregulation ofFrontiers in endocrinology · 2021Article
- Developmental Time Course of SNAP-25 Isoforms Regulate Hippocampal Long-Term Synaptic Plasticity and Hippocampus-Dependent Learning.International journal of molecular sciences · 2020Article
- Dietary Exposure to Excess Saturated Fat During Early Life Alters Hippocampal Gene Expression and Increases Risk for Behavioral Disorders in Adulthood.Frontiers in neuroscience · 2020Article
- Modelling of dysregulated glucagon secretion in type 2 diabetes by considering mitochondrial alterations in pancreatic α-cells.Royal Society open science · 2020Article
- Disabling Gβγ-SNAP-25 interaction in gene-targeted mice results in enhancement of long-term potentiation at Schaffer collateral-CA1 synapses in the hippocampus.Neuroreport · 2019Article
- SNAP-25 isoforms differentially regulate synaptic transmission and long-term synaptic plasticity at central synapses.Scientific reports · 2019Article
- How alternative splicing affects membrane-trafficking dynamics.Journal of cell science · 2018Review
- New Insights Into Interactions of Presynaptic Calcium Channel Subtypes and SNARE Proteins in Neurotransmitter Release.Frontiers in molecular neuroscience · 2018Article
- SNAP-25b-deficiency increases insulin secretion and changes spatiotemporal profile of CaScientific reports · 2017Article
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptosomal-associated protein of 25 kDa (SNAP-25) is a key molecule in the soluble N-ethylmaleimide-sensitive factor attachment protein (SNARE) complex mediating fast Ca(2+)-triggered release of hormones and neurotransmitters, and both splice variants, SNAP-25a and SNAP-25b, can participate in this process. Here we explore the hypothesis that minor alterations in the machinery mediating regulated membrane fusion can increase the susceptibility for metabolic disease and precede obesity and type 2 diabetes. Thus, we used a mouse mutant engineered to express normal levels of SNAP-25 but only SNAP-25a. These SNAP-25b-deficient mice were exposed to either a control or a high-fat/high-sucrose diet. Monitoring of food intake, body weight, hypothalamic function, and lipid and glucose homeostases showed that SNAP-25b-deficient mice fed with control diet developed hyperglycemia, liver steatosis, and adipocyte hypertrophy, conditions dramatically exacerbated when combined with the high-fat/high-sucrose diet. Thus, modified SNARE function regulating stimulus-dependent exocytosis can increase the vulnerability to and even provoke metabolic disease. When combined with a high-fat/high-sucrose diet, this vulnerability resulted in diabesity. Our SNAP-25b-deficient mouse may represent a diabesity model.
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