Abstract
Metabolic syndrome (MS) is a chronic pathology characterized (amongst others) by dysregulated plasma glucose and high serum triglycerides. One of the central organs affected is the liver, causing increasing fat accumulation and inflammation. To investigate the impact of chronic inflammation and fat accumulation on the main mammalian proteolytic and -static system – the ubiquitin-proteasomal system (UPS) – the liver of NZO mice suffering either from hyperlipidemia or from both hyperlipidemia and hyperglycemia at different ages was investigated. Our interest was in changes/redistributions of UPS-compounds (depending on age and/or metabolic state) as well as its response to the chronic inflammation associated with MS. First experimental results revealed changes in the distribution of UPS-compounds (especially of its central protease, the 20 S proteasome, responsible for proteolytic degradation of oxidatively damaged proteins) as well as expression of the so-called “immunoproteasome” (i20S), a special form induced by inflammation. Furthermore, the proteasomal 19 S regulator (enabling degradation of native proteins) was significantly redistributed between nucleus and cytosol of the investigated liver cells, as well as the amounts of oxidatively damaged proteins. Summarizing our results, we hypothesize that the cellular dysfunctions induced by MS are in part due to changes of the UPS.
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