What question did this study set out to answer?

This research aims to understand how the loss of AKT signaling affects lipid metabolism and heart function in cardiac myocytes.

April 15, 2026MetabolismOpen Access

Simultaneous deletion of cardiomyocyte AKT1 and AKT2 in mice induced lethal heart failure and energetic depletion, evidenced by a drop in cardiac phosphocreatine/ATP ratios from 2 to 1.5.

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Authors

SGStefanie Gödecke AHAndré Heinen TATim Appel

Discussion

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Overview

Investigations reveal that loss of AKT signaling disrupts lipid metabolism in cardiac myocytes, suggesting critical roles for heart health.

Key Points

This research aims to understand how the loss of AKT signaling affects lipid metabolism and heart function in cardiac myocytes.
Utilized inducible cardiomyocyte-specific AKT1 AKT2 double knockout mice.
Performed metabolic analyses using respirometry and Seahorse flux analysis on cardiac tissue.
Conducted in vivo NMR spectroscopy and CrCEST imaging to assess cardiac energetics.
Executed transcriptomic and proteomic studies to analyze gene expression related to metabolism.
Double knockout mice exhibited rapid heart failure and cardiomyocyte atrophy.
Fatty acid metabolism significantly declined, while glucose metabolism was relatively maintained.
Cardiac phosphocreatine/ATP ratios decreased from 2 to 1.5, indicating energy depletion.
Key metabolic genes involved in the TCA cycle and oxidative phosphorylation were down-regulated.
Loss of perilipins and associated proteins led to decreased ability to store fatty acids in lipid droplets.

Cite This Study

Gödecke et al. (2026) studied this question. Simultaneous deletion of cardiomyocyte AKT1 and AKT2 in mice induced lethal heart failure and energetic depletion, evidenced by a drop in cardiac phosphocreatine/ATP ratios from 2 to 1.5.

synapsesocial.com/papers/69df2a4be4eeef8a2a6af743 https://doi.org/10.1016/j.metabol.2026.156619

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April 15, 2026MetabolismOpen Access

Simultaneous deletion of cardiomyocyte AKT1 and AKT2 in mice induced lethal heart failure and energetic depletion, evidenced by a drop in cardiac phosphocreatine/ATP ratios from 2 to 1.5.

View Full Paper

Ask AI

Bookmark

Key result

Simultaneous deletion of cardiomyocyte AKT1 and AKT2 in mice induced lethal heart failure and energetic depletion, evidenced by a drop in cardiac phosphocreatine/ATP ratios from 2 to 1.5.

Authors

SGStefanie Gödecke AHAndré Heinen TATim Appel

Discussion

Member takes

Overview

Investigations reveal that loss of AKT signaling disrupts lipid metabolism in cardiac myocytes, suggesting critical roles for heart health.

Key Points

This research aims to understand how the loss of AKT signaling affects lipid metabolism and heart function in cardiac myocytes.
Utilized inducible cardiomyocyte-specific AKT1 AKT2 double knockout mice.
Performed metabolic analyses using respirometry and Seahorse flux analysis on cardiac tissue.
Conducted in vivo NMR spectroscopy and CrCEST imaging to assess cardiac energetics.
Executed transcriptomic and proteomic studies to analyze gene expression related to metabolism.
Double knockout mice exhibited rapid heart failure and cardiomyocyte atrophy.
Fatty acid metabolism significantly declined, while glucose metabolism was relatively maintained.
Cardiac phosphocreatine/ATP ratios decreased from 2 to 1.5, indicating energy depletion.
Key metabolic genes involved in the TCA cycle and oxidative phosphorylation were down-regulated.
Loss of perilipins and associated proteins led to decreased ability to store fatty acids in lipid droplets.

Cite This Study

synapsesocial.com/papers/69df2a4be4eeef8a2a6af743 https://doi.org/10.1016/j.metabol.2026.156619

View Full Paper

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