The Study
Low glucose stress decreases cellular NADH and mitochondrial ATP in colonic epithelial cancer cells: Influence of mitochondrial substrates
This study watched how cancer cells in a petri dish reacted when scientists changed their food (glucose) and gave them extra snacks (malate, succinate). It saw some changes in how the cells made energy, but it didn't prove that one thing caused another — just that they happened together.
Analysis score
Maximum 44 for a cross-sectional study.
Where the score came from
When cancer cells don't get enough sugar, they struggle to make energy and produce less lactate. But adding malate and glutamate helps them bounce back — like giving them a backup fuel.
Where does this study sit?
Reviews of RCTs (Meta-analyses)
Max 100Randomized Trials
Max 90Reviews of Cohort Studies
Max 85Cohort Studies
Max 72Reviews of Case-Control Studies
Max 63Case-Control Studies
Max 58Cross-Sectional & Case Series
Max 50Expert Opinion
Max 56 / 100
Quality score
Snapshots of a population at a single point in time, or descriptions of small groups. Can identify correlations and prevalence, but cannot determine cause and effect.
Key takeaways
Summary
Based on the study abstract and findings.
- 1Yes — this shows cancer cells can switch fuel sources to survive low sugar, which might help them resist treatments that starve them of glucose.
- 2Low sugar: NADH dropped, lactate dropped 20%, mitochondrial ATP dropped 20%, glycolytic ATP rose 15–20%.
- 3Malate+glutamate restored lactate to normal levels; succinate did nothing.
Score breakdown, methodology, conflicts of interest, evidence analysis & raw study data
Publication
Journal
Chemico-biological interactions
Year
2017
Authors
M. Circu, R. Maloney, T. Aw
Related Content
Claims (5)
When HT29 colon cancer cells are exposed to low glucose, their mitochondrial ATP production decreases by about 20%, and their glycolytic ATP production increases by 15–20%, resulting in a measurable shift from mitochondrial energy production to glycolysis.
In HT29 colon cancer cells, adding malate and glutamate raises NADH levels in the cytoplasm and mitochondria when glucose is normal, but under low glucose, it raises cytoplasmic NAD+ and lowers the NADH-to-NAD+ ratio, showing different metabolic responses in different cell compartments.
In HT29 colon cancer cells, adding succinate increases the rate at which mitochondria consume oxygen under normal glucose and high oxygen conditions, but does not increase the amount of ATP produced, showing that oxygen use and energy production are no longer linked.
When HT29 human colon cancer cells are deprived of glucose at 1.1 mM, their NADH levels drop, NAD+ levels rise, the NADH/NAD+ ratio falls, lactate production decreases, and lactate dehydrogenase activity is reduced, indicating a suppression of aerobic glycolysis.
In HT29 colon cancer cells grown with low glucose, adding malate and glutamate restores lactate production, but adding succinate does not, showing that malate breakdown sustains lactate generation when glucose is scarce.
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.