Key result
Severe PAH in rats impairs RV metabolism via decreased TCA cycle and fatty acid oxidation.
Why the study?
Although fatty acid and glucose accumulate in the right ventricle in pulmonary hypertension, the details of metabolic remodeling remain to be elucidated.
Does the Su/Hx model of severe pulmonary arterial hypertension induce metabolic remodeling in the right ventricle of rats?
Population
Male rats
Comparison
SU5416 plus hypoxia followed by normoxia (Su/Hx rats) vs controls
Design
Animal experimental study
Authors
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Impaired FA oxidation and BCAA dysregulation may reduce TCA activity in severe PH rat RV without glycolysis shift; leaves open therapeutic targets pending human data.
Does the Su/Hx model of severe pulmonary arterial hypertension induce metabolic remodeling in the right ventricle of rats?
In a rat model of severe pulmonary arterial hypertension, right ventricular metabolic remodeling is characterized by reduced TCA cycle activity and fatty acid oxidation, alongside dysregulated branched-chain amino acid metabolism, rather than altered glycolysis.
Sakao et al. (2021) studied Severe pulmonary arterial hypertension (n=6). SU5416 followed by hypoxia and normoxia (Su/Hx model) vs. Untreated controls was evaluated on Metabolite concentrations in the right ventricle (TCA cycle intermediates, BCAAs, long-chain acylcarnitines). In a rat model of severe pulmonary arterial hypertension, the right ventricle exhibited a less active TCA cycle, dysregulated branched-chain amino acid metabolism, and decreased fatty acid oxidation.