What is the clinical evidence from this study?

Intervention: C14-labeled pyruvate. Primary outcome: Pyruvate metabolism (decarboxylation, lactate formation, lipid incorporation).

What question did this study set out to answer?

To determine the metabolic pathways of pyruvate in perfused myocardial tissue and examine its reciprocal interactions with fatty acid utilization during fed and fasting states.

November 1, 1963American Journal of Physiology-Legacy Content

Pyruvate metabolism in the perfused rat heart

View Full Paper

Ask AI

Bookmark

Key result

In the isolated perfused rat heart, decarboxylation was the major fate of pyruvate, which was reduced in hearts from fasted rats compared to those fed ad libitum.

Population

Isolated perfused rat hearts (from rats fed ad libitum and fasted overnight)

Comparison

Perfusion with C14-labeled pyruvate at varying… vs Fasted versus fed state; varying concentrations…

Design

Preclinical

Authors

JEJohn R. EvansSwinburne University of Technology LOLionel H. OpieGeneral Cardiology ARAlbert E. RenoldUniversity of Geneva

Discussion

Member takes

Implication

Rat heart findings on fasting and pyruvate use warrant caution in clinical translation; leaves open fatty acid oxidation mechanisms in human myocardium.

Key Points

To determine the metabolic pathways of pyruvate in perfused myocardial tissue and examine its reciprocal interactions with fatty acid utilization during fed and fasting states.
Perfused isolated rat hearts in a closed recirculation system using carbon-14-labeled pyruvate (pyruvate-1-C14 and pyruvate-2-C14).
Measured oxidation and tissue triglyceride incorporation of palmitate-C14 in the presence of 5 mM and 10 mM pyruvate concentrations, comparing hearts from fed versus overnight-fasted rats.
Decarboxylation was the principal fate of pyruvate-1-C14, increasing in proportion to perfusion concentration, while lactate formation accounted for the remaining uptake with negligible radioactivity in tissue lipids or glycogen.
Pyruvate at 5 mM and 10 mM concentrations inhibited palmitate-C14 oxidation and increased its incorporation into tissue triglycerides.
Pyruvate-1-C14 uptake and decarboxylation were markedly lower in hearts from overnight-fasted rats than in hearts from fed rats.

Structured PICO

Population

Isolated perfused rat hearts used to study the metabolism of C14-labeled pyruvate.

Intervention

Perfusion with C14-labeled pyruvate (pyruvate-1-C14 and pyruvate-2-C14) at varying concentrations (including 5- and 10-mm) and palmitate-C14

Comparator

Fasted versus fed state; varying concentrations of pyruvate

Outcome

Metabolic fate of pyruvate (decarboxylation, lactate formation, lipid/glycogen incorporation) and effect on palmitate oxidationsurrogate

Fatty acid oxidation may be the mechanism responsible for decreased myocardial utilization of pyruvate in the fasting state and other conditions where fatty acid is the principal fuel.

Cite This Study

Evans et al. (1963) studied this question. C14-labeled pyruvate was evaluated on Pyruvate metabolism (decarboxylation, lactate formation, lipid incorporation). In the isolated perfused rat heart, decarboxylation was the major fate of pyruvate, which was reduced in hearts from fasted rats compared to those fed ad libitum.

synapsesocial.com/papers/6a92a9a764e69d4ef34672d3 https://doi.org/10.1152/ajplegacy.1963.205.5.971

View Full Paper

Ask AI

Bookmark

Implication

Rat heart findings on fasting and pyruvate use warrant caution in clinical translation; leaves open fatty acid oxidation mechanisms in human myocardium.

Pyruvate metabolism in the perfused rat heart

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Pyruvate metabolism in the perfused rat heart

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider