Madlala 2019 Integr Food Nutr Metab
|Madlala HP, Maarman GJ, Ojuka E (2019) Fructose impairs mitochondrial respiration and substrate utilization in hepatocytes via the enzyme, glutamate oxaloacetate transaminase. Integr Food Nutr Metab doi: 10.15761/IFNM.1000228.|
Abstract: Excess fructose associates with increased production of reactive oxygen species (ROS) that inhibits enzymes such as aconitase, which should affect mitochondrial metabolism. Yet there is a lack of studies investigating the impact of excess fructose on mitochondrial metabolic pathways and substrate utilization. We evaluated the impact of excess fructose on hepatocyte mitochondrial enzymes; citrate synthase (CS), aconitase and glutamate-oxaloacetate transaminase (GOT). Also, high-resolution using complex I-linked substrates [pyruvate+malate (PM), glutamate+malate (GM) and PGM]. Fructose decreased the activities of aconitase and GOT by 35% and 47% respectively. Respiration at Leak, OXPHOS and ETS states were reduced with GM but not PM or PGM. Thus, excess fructose inhibits GOT activity, reduced mitochondrial leak respiration, OXPHOS and ETS capacity. These changes were observed with complex-1 linked respiration (substrates GM). Therefore, fructose impairs mitochondrial respiration and substrate utilization via the enzyme GOT.
Labels: MiParea: Respiration
Organism: Human Tissue;cell: Liver Preparation: Permeabilized cells
Regulation: Inhibitor, Substrate Coupling state: LEAK, OXPHOS, ET Pathway: N, CIV, ROX HRR: Oxygraph-2k