ArticlePloS one2016
Mimp/Mtch2, an Obesity Susceptibility Gene, Induces Alteration of Fatty Acid Metabolism in Transgenic Mice.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- The conserved outer mitochondrial membrane protein Mtch regulates mitophagy during Drosophila intestinal development.PLoS biology · 2026Article
- Review
- MTCH2 modulates CPT1 activity to regulate lipid metabolism of adipocytes.Nature communications · 2025Article
- MTCH2 Deficiency Promotes E2F4/TFRC-Mediated Ferroptosis and Sensitizes Colorectal Cancer Liver Metastasis to Sorafenib.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Interplay of Genetic Predisposition, Circadian Misalignment, and Metabolic Regulation in Obesity.Current obesity reports · 2025Review
- Multiple entanglements of different cell death pathways, in which caspase-8 and BID interact with cardiolipin*, have been identified.Frontiers in cell and developmental biology · 2025Review
- MTCH2 cooperates with MFN2 and lysophosphatidic acid synthesis to sustain mitochondrial fusion.EMBO reports · 2024Article
- MTCH2 in Metabolic Diseases, Neurodegenerative Diseases, Cancers, Embryonic Development and Reproduction.Drug design, development and therapy · 2024Review
- Opposing effects of genetic variation in MTCH2 for obesity versus heart failure.Human molecular genetics · 2023Article
- Evidence for correlations between BMI-associated SNPs and circRNAs.Scientific reports · 2022Article
- Positively selected genes in the hoary bat (PeerJ · 2022Article
- The modified mitochondrial outer membrane carrier MTCH2 links mitochondrial fusion to lipogenesis.The Journal of cell biology · 2021Article
- Stop codon read-through of mammalianThe Journal of biological chemistry · 2020Article
- Computational analyses of obesity associated loci generated by genome-wide association studies.PloS one · 2018Article
- Non-apoptotic functions of BCL-2 family proteins.Cell death and differentiation · 2017Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveMetabolic dysfunctions, such as fatty liver, obesity and insulin resistance, are among the most common contemporary diseases worldwide, and their prevalence is continuously rising. Mimp/Mtch2 is a mitochondrial carrier protein homologue, which localizes to the mitochondria and induces mitochondrial depolarization. Mimp/Mtch2 single-nucleotide polymorphism is associated with obesity in humans and its loss in mice muscle protects from obesity. Our aim was to study the effects of Mimp/Mtch2 overexpression in vivo.
methodsTransgenic mice overexpressing Mimp/Mtch2-GFP were characterized and monitored for lipid accumulation, weight and blood glucose levels. Transgenic mice liver and kidneys were used for gene expression analysis.
resultsMimp/Mtch2-GFP transgenic mice express high levels of fatty acid synthase and of β-oxidation genes and develop fatty livers and kidneys. Moreover, high-fat diet-fed Mimp/Mtch2 mice exhibit high blood glucose levels. Our results also show that Mimp/Mtch2 is involved in lipid accumulation and uptake in cells and perhaps in human obesity.
conclusionsMimp/Mtch2 alters lipid metabolism and may play a role in the onset of obesity and development of insulin resistance.
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