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Bachelor Thesis from the year 2010 in the subject Biology - Micro- and Molecular Biology, grade: 2,0, FH Campus Vienna - University of Applied Sciences (Molekulare Biotechnologie), language: English, abstract: Chronic Heart Failure (CHF) is combined with various metabolic shifts. The continuous adrenergic stress results in a metabolic shift increasing glycolysis similar to a fetal metabolism. However also insulin resistance (IR) was reported triggering low glucose uptake and mitochondrial uncoupling and therefore reactive oxygen species (ROS) production reduce cardiac contractility. The adrenergic increased free fatty acids (FFA) are metabolized to ketone bodies (mainly beta-hydroxybutyrate (OHB)) which are also energy stocks for brain and heart. Elevated blood ketone levels have been reported during CHF similar to diabetes. Clinically a correlation between ketone body blood level and severity of CHF has been discovered. However it remains unclear whether this is a result of metabolic changes or a compensatory mechanism. The aim of this study was to show, that rat cardiomyocytes (H9c2) treated with Phenylephrine (PE) for hypertrophy are slightly more susceptible to OHB at concentrations similar found in patients with CHF and that OHB reduces cell area significantly.
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