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  • Mitochondrial oxidative phosphorylation (OXPHOS) provides most of energy in mammalian cells and tissues. OXPHOS system is uniquely encoded by both nuclear and mitochondrial genes. Dysfunction of OXPHOS are known to cause numerous types of mitochondrial diseases. Mitochondrial malfunction is also expected to play a role in complex metabolic diseases such as metabolic syndrome, however the respective mitochondrial genetic determinants are largely unknown. The aim of the project is to characterize the role of mitochondrial OXPHOS system and mitochondrial genome in pathogenesis of metabolic syndrome. The project is based on the use of unique model of rat conplastic strains with identical nuclear genome but different haplotypes of mitochondrial DNA and on detailed characterization of metabolic phenotypes together with analysis of changes in structure and function of OXPHOS system with respect to mitochondrial energy conversion and ROS production. (en)
  • Cílem projektu je přispět k poznání úlohy mitochondrií a mitochondriálního genomu v patogenezi a fenotypických projevech metabolického syndromu.
Title
  • The mitochondrial genome and oxidative phosphorylation system in metabolic syndrome (en)
  • Mitochondriální genom a oxidačně fosforylační systém u metabolického syndromu
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  • OC08017
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  • mitochondria mitochondrial DNA oxidative phosphorylation rat conplastic strains metabolic syndrome bioactive food component ATP ROS (en)
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  • Byly připraveny SHR-konplastické potkaní kmeny s různými haplotypy mitochondriální mtDNA. Studie mitochondriálního oxidačně fosforylačního aparátu a metabolických fenotypů prokázaly, že dědičné změny v mtDNA při absenci změn v jaderném genomu mohou tkáňově specificky ovlivňovat disposici k metabolickému syndromu. Analýzy CD36/FAT permeázy prokázaly její extramitochondriální lokalisaci. (cs)
  • Conplastic strains with different haplotypes of mitochondrial mtDNA have been derived from SHR rats. Studies on mitochondrial oxidative phosphorylation system and metabolic phenotypes revealed that inherited changes in mtDNA without changes in nuclear genome may predispose to metabolic syndrome in a tissue specific manner. Analysis of CD36/FAT permease showed its extramitochondrial location. (en)
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