Abstract
Fructose impairs mitochondrial respiration and substrate utilization in hepatocytes via the enzyme, glutamate oxaloacetate transaminase
Highlights
There are increasing health concerns about the excess consumption of fructose in the form of high fructose corn syrup in modern diets [1]
Fructose had no influence on the activity of citrate synthase after 72-hour exposure (Figure 1A)
Fructose did not affect complex 4-oxygen flux, which was consistent throughout all experiments and used as normalising factor for respiratory data
Summary
There are increasing health concerns about the excess consumption of fructose in the form of high fructose corn syrup in modern diets [1]. The first step in this pathway is the phosphorylation of fructose, to fructose 1-phosphate by the high affinity ketohexokinase (fructokinase) enzyme. Because this reaction has a low Michaelis constant, and is not controlled allosterically or hormonally, plasma fructose is rapidly cleared and adenosine triphosphate (ATP) inside the hepatocyte is rapidly depleted [3]. There is a lack of studies providing extended investigation into the impact of excess fructose on mitochondrial metabolic pathways and substrate utilization. Such investigations is important, as the data generated could build upon previous research, and contribute to the body of knowledge on the adverse metabolic effects of excess fructose. The aim of this study was to investigate the effects of excess fructose on mitochondrial metabolic pathways and substrate utilization
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