| First Author | Bar-Lev Y | Year | 2016 |
| Journal | PLoS One | Volume | 11 |
| Issue | 6 | Pages | e0157850 |
| PubMed ID | 27359329 | Mgi Jnum | J:249266 |
| Mgi Id | MGI:6094342 | Doi | 10.1371/journal.pone.0157850 |
| Citation | Bar-Lev Y, et al. (2016) Mimp/Mtch2, an Obesity Susceptibility Gene, Induces Alteration of Fatty Acid Metabolism in Transgenic Mice. PLoS One 11(6):e0157850 |
| abstractText | 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 beta-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. |
