Mechanisms of control of heart glycolysis.
Level 5 - mechanism / opinion, no new human data
Narrative review of biochemical mechanisms without systematic search methodology or new human data
PubMed 9874192 · doi:10.1046/j.1432-1327.1998.2580277.x
What was done
This narrative review synthesizes biochemical and kinetic properties of key regulatory steps in cardiac glycolysis—including glucose transporters, hexokinase, glycogen phosphorylase, and phosphofructokinases. It examines how substrate supply, energy demand, hormonal signaling (insulin, adrenaline), and oxygen deprivation control glycolytic flux and fuel selection in the heart, focusing on the regulatory roles of fructose 2,6-bisphosphate, cyclic AMP, nitric oxide, and cyclic GMP.
What was found
The abstract reports no numerical values or quantitative effect sizes. It describes that fructose 2,6-bisphosphate acts as a glycolytic signal that stimulates glycolysis in response to glucose, workload, insulin, and adrenaline, and decreases flux when alternative fuels are oxidized. Adrenaline and cyclic AMP relieve fuel-mediated inhibition of glycolysis while stimulating fatty acid oxidation, whereas insulin and glucose stimulate glycolysis and inhibit fatty acid oxidation. Nitric oxide and cyclic GMP are implicated in metabolic adaptation to oxygen deprivation.
Why it matters
This paper delineates the biochemical control points and signaling hierarchies governing myocardial fuel selection, providing a framework for understanding metabolic shifts during cardiac workload changes and ischemic stress.
Limits
As a narrative review, it lacks a systematic search protocol, quality assessment of included studies, and primary experimental data. No sample size, quantitative metrics, or clinical human outcome data are provided in the abstract.
Cited by
- supports Carbohydrate restriction and low insulin levels inhibit glycolytic enzymes like hexokinase and promote internalization of glucose transporters.