What question did this study set out to answer?

To investigate whether augmented ketone body metabolism mediated by Bdh1 expression protects the heart against pressure overload–induced failure.

December 1, 2017Circulation Heart Failure

Cardiac-Specific Bdh1 Overexpression Ameliorates Oxidative Stress and Cardiac Remodeling in Pressure Overload–Induced Heart Failure

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Why the study?

Does cardiac-specific Bdh1 overexpression prevent cardiac remodeling and oxidative stress in pressure overload-induced heart failure models?

Population

Heart-specific Bdh1-overexpressing transgenic mice and in vitro cell models subjected to transverse aortic…

Comparison

Cardiac-specific Bdh1 overexpression vs Wild-type or control mice/cells

Design

Preclinical

Authors

MUMotoki UchihashiSaiseikai Shigaken Hospital AHAtsushi HoshinoKyoto Prefectural University of Medicine YOYoshifumi OkawaKyoto Medical Center

Discussion

Member takes

Implication

Hypothesis-generating for Bdh1 modulation in pressure-overload HF; human studies required before clinical consideration.

Key Points

To investigate whether augmented ketone body metabolism mediated by Bdh1 expression protects the heart against pressure overload–induced failure.
Quantified cardiac Bdh1 expression and ketone body oxidation via microarray, iTRAQ proteomics, and radiolabeled [1-14C] β-hydroxybutyrate assays in mice subjected to transverse aortic constriction (TAC).
Generated heart-specific Bdh1-overexpressing transgenic mice subjected to TAC to evaluate cardiac fibrosis, contractility, and oxidative stress markers.
Evaluated rotenone-induced reactive oxygen species production and hydrogen peroxide–induced apoptosis in vitro using adenovirus-mediated Bdh1 overexpression.
TAC induced a 2.5-fold and 2.8-fold increase in Bdh1 expression by microarray and proteomics, respectively, alongside a 2.2-fold upregulation in ketone body oxidation.
Bdh1 transgenic mice displayed a 1.7-fold increase in basal ketone body oxidation and exhibited marked resistance to TAC-induced fibrosis, contractile dysfunction, and protein carbonylation.
Adenovirus-mediated Bdh1 overexpression suppressed rotenone-induced reactive oxygen species generation and significantly attenuated hydrogen peroxide–induced apoptosis in vitro.

Structured PICO

Does cardiac-specific Bdh1 overexpression prevent cardiac remodeling and oxidative stress in pressure overload-induced heart failure models?

Population

Heart-specific Bdh1-overexpressing transgenic mice and in vitro cell models subjected to transverse aortic constriction or oxidative stress

Intervention

Cardiac-specific Bdh1 overexpression

Comparator

Wild-type or control mice/cells

Outcome

Fibrosis, contractile dysfunction, and oxidative damagesurrogate

Increased ketone body utilization via Bdh1 overexpression protects against oxidative stress and cardiac remodeling in a murine model of pressure overload-induced heart failure.

Cite This Study

Uchihashi et al. (2017) studied this question.

synapsesocial.com/papers/6a7df800629c956ef7ac8ccf https://doi.org/10.1161/circheartfailure.117.004417

Topics

Heart failure HFrEF treatment

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Cardiac-Specific Bdh1 Overexpression Ameliorates Oxidative Stress and Cardiac Remodeling in Pressure Overload–Induced Heart Failure

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Cardiac-Specific Bdh1 Overexpression Ameliorates Oxidative Stress and Cardiac Remodeling in Pressure Overload–Induced Heart Failure

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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