Stankova, Pavla published the artcileAdaptation of mitochondrial substrate flux in a mouse model of nonalcoholic fatty liver disease, Synthetic Route of 97-67-6, the main research area is mitochondrial substrate flux nonalcoholic fatty liver disease adaptation animal; mitochondria; nonalcoholic fatty liver disease; oxidative phosphorylation; respirometry.
Maladaptation of mitochondrial oxidative flux seems to be a considerable feature of nonalcoholic fatty liver disease (NAFLD). The aim of this work was to induce NAFLD in mice fed a Western-style diet (WD) and to evaluate liver mitochondrial functions. Experiments were performed on male C57BL/6J mice fed with a control diet or a WD for 24 wk. Histol. changes in liver and adipose tissue as well as hepatic expression of fibrotic and inflammatory genes and proteins were evaluated. The mitochondrial respiration was assessed by high-resolution respirometry. Oxidative stress was evaluated by measuring lipoperoxidation, glutathione, and reactive oxygen species level. Feeding mice a WD induced adipose tissue inflammation and massive liver steatosis accompanied by mild inflammation and fibrosis. We found decreased succinate-activated mitochondrial respiration and decreased succinate dehydrogenase (SDH) activity in the mice fed a WD. The oxidative flux with other substrates was not affected. We observed increased ketogenic capacity, but no impact on the capacity for fatty acid oxidation We did not confirm the presence of oxidative stress. Mitochondria in this stage of the disease are adapted to increased substrate flux. However, inhibition of SDH can lead to the accumulation of succinate, an important signaling mol. associated with inflammation, fibrosis, and carcinogenesis.
International Journal of Molecular Sciences published new progress about Adaptation. 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Synthetic Route of 97-67-6.
Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts