July 26, 2013PLoS ONEOpen Access

AMPK-Regulated and Akt-Dependent Enhancement of Glucose Uptake Is Essential in Ischemic Preconditioning-Alleviated Reperfusion Injury

Q: What is the clinical evidence from this study?

Study design: Other. Population: Myocardial ischemia/reperfusion injury. Intervention: Ischemic preconditioning (IPC) vs. Ischemia/reperfusion without preconditioning. Primary outcome: Myocardial glucose uptake and infarct size (p=<0.01).

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Key result

Ischemic preconditioning significantly improved myocardial glucose uptake and reduced reperfusion injury via co-activation of AMPK and Akt, a protective mechanism that was absent in diabetic rats but restorable with insulin.

Population

Adult male Sprague-Dawley rats, either normal or streptozotocin-induced insulin-deficient diabetic.

Comparison

Ischemic preconditioning consisting of 2 cycles… vs Myocardial ischemia/reperfusion without ischemic…

Design

Preclinical, randomly assigned, blinded manner

Follow-up

up to 3 hours of reperfusion

Authors

LJLele JiAir Force Medical University XZXing ZhangSouthwest University WLWenchong LiuJilin Agricultural University

Discussion

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Implication

Hypothesis-generating for insulin to restore preconditioning in diabetes; leaves open clinical translation from this animal model.

Structured PICO

Population

Adult male Sprague-Dawley rats, including normal and STZ-induced diabetic models, subjected to in vivo myocardial ischemia and reperfusion.

Intervention

Ischemic preconditioning (IPC) consisting of 2 cycles of 5 min ischemia and 5 min reperfusion prior to 30 min of myocardial ischemia and 3 h of reperfusion. Additional interventions in subgroups included intramyocardial GLUT4 siRNA, intravenous PI3K inhibitor wortmannin (15 mg/kg), or intravenous insulin (60 U/L at 4 mL/kg per hour).

Comparator

Myocardial ischemia/reperfusion (MI/R) without ischemic preconditioning, or sham-operated controls.

Outcome

Myocardial glucose uptake at 1 hour of reperfusion (measured by 18F-FDG PET and gamma-counter biodistribution) and myocardial infarct size/apoptosis at 3 hours of reperfusion.surrogate

Main Result

p-value: p=<0.01

Ischemic preconditioning protects against reperfusion injury by enhancing myocardial glucose uptake via AMPK and Akt co-activation, a mechanism that is blunted in diabetes but can be restored with exogenous insulin.

Limitations

STZ-induced diabetes model is complex and introduces multiple metabolic confounders (e.g., increased free fatty acids, cholesterol, triglycerides).
The direct causal relation whereby insulin signaling promotes the metabolic modulation of IPC remains largely associative.

Cite This Study

Ji et al. (2013) studied Myocardial ischemia/reperfusion injury. Ischemic preconditioning (IPC) vs. Ischemia/reperfusion without preconditioning was evaluated on Myocardial glucose uptake and infarct size (p=<0.01). Ischemic preconditioning significantly improved myocardial glucose uptake and reduced reperfusion injury via co-activation of AMPK and Akt, a protective mechanism that was absent in diabetic rats but restorable with insulin.

synapsesocial.com/papers/6a99af18a5163385d4e6c072 https://doi.org/10.1371/journal.pone.0069910

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AMPK-Regulated and Akt-Dependent Enhancement of Glucose Uptake Is Essential in Ischemic Preconditioning-Alleviated Reperfusion Injury

Discussion

Member takes

Implication

Structured PICO

Main Result

Limitations

Cite This Study

AMPK-Regulated and Akt-Dependent Enhancement of Glucose Uptake Is Essential in Ischemic Preconditioning-Alleviated Reperfusion Injury

Discussion

Member takes

Implication

Structured PICO

Main Result

Limitations

Cite This Study

Also Consider

Also Consider