title: Mimp/Mtch2, an Obesity Susceptibility Gene, Induces Alteration of Fatty Acid Metabolism in Transgenic Mice.
abstract: OBJECTIVE
  Metabolic 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.
  
  
  METHODS
  Transgenic 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.
  
  
  RESULTS
  Mimp/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.
  
  
  CONCLUSIONS
  Mimp/Mtch2 alters lipid metabolism and may play a role in the onset of obesity and development of insulin resistance.
authors.affiliation: Department of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
authors.forename: Yamit
authors.initials: Y
authors.lastname: Bar-Lev
authors.affiliation: Cancer Research Center, Sheba Medical Center, Ramat-Gan, Israel.
authors.forename: Sharon
authors.initials: S
authors.lastname: Moshitch-Moshkovitz
authors.affiliation: Department of Diagnostic Imaging, Sheba Medical Center, Ramat-Gan, Israel.
authors.forename: Galia
authors.initials: G
authors.lastname: Tsarfaty
authors.affiliation: Van Andel Research Institute, Grand Rapids, Michigan, 49503, United States of America.
authors.forename: Dafna
authors.initials: D
authors.lastname: Kaufman
authors.affiliation: Department of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
authors.forename: Judith
authors.initials: J
authors.lastname: Horev
authors.affiliation: Van Andel Research Institute, Grand Rapids, Michigan, 49503, United States of America.
authors.forename: James H
authors.initials: JH
authors.lastname: Resau
authors.affiliation: Department of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
authors.forename: Ilan
authors.initials: I
authors.lastname: Tsarfaty
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D059305:Diet, High-Fat; D064429:Fatty Acid Synthases / Q000235:genetics; D020869:Gene Expression Profiling / Q000379:methods*; D005786:Gene Expression Regulation; D007668:Kidney / Q000378:metabolism / Q000473:pathology*; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism / Q000473:pathology*; D053078:Membrane Potential, Mitochondrial; D051379:Mice; D008822:Mice, Transgenic; D033681:Mitochondrial Membrane Transport Proteins / Q000235:genetics* / Q000378:metabolism; D009765:Obesity / Q000235:genetics*; D020411:Oligonucleotide Array Sequence Analysis / Q000379:methods*
chemical_list: D001786:Blood Glucose; D033681:Mitochondrial Membrane Transport Proteins; C550380:Mtch2 protein, mouse; D064429:Fatty Acid Synthases