Increased Glycolysis and Higher Lactate Production in Hyperglycemic Myotubes.
Jenny LundD Margriet OuwensMarianne WettergreenSiril S BakkeG Hege ThoresenVigdis AasPublished in: Cells (2019)
Previous studies have shown that chronic hyperglycemia impairs glucose and fatty acid oxidation in cultured human myotubes. To further study the hyperglycemia-induced suppression of oxidation, lactate oxidation, mitochondrial function and glycolytic rate were evaluated. Further, we examined the intracellular content of reactive oxygen species (ROS), production of lactate and conducted pathway-ANOVA analysis on microarray data. In addition, the roles of the pentose phosphate pathway (PPP) and the hexosamine pathway were evaluated. Lactic acid oxidation was suppressed in hyperglycemic versus normoglycaemic myotubes. No changes in mitochondrial function or ROS concentration were observed. Pathway-ANOVA analysis indicated several upregulated pathways in hyperglycemic cells, including glycolysis and PPP. Functional studies showed that glycolysis and lactate production were higher in hyperglycemic than normoglycaemic cells. However, there were no indications of involvement of PPP or the hexosamine pathway. In conclusion, hyperglycemia reduced substrate oxidation while increasing glycolysis and lactate production in cultured human myotubes.
Keyphrases
- reactive oxygen species
- endothelial cells
- hydrogen peroxide
- induced apoptosis
- diabetic rats
- fatty acid
- cell cycle arrest
- cell death
- lactic acid
- dna damage
- type diabetes
- high glucose
- nitric oxide
- blood pressure
- induced pluripotent stem cells
- adipose tissue
- drug induced
- big data
- artificial intelligence
- insulin resistance
- weight loss