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This metabolic shift was clearly induced by a small electron uptake that represented less than 0.6% of the electrons consumed by C. pasteurianum.
Therefore it is likely that such a metabolic shift was also involved in our fermentation tests.
Gene expression profiling of the S. epidermidis biofilm was analyzed and some significant metabolic shift was found between the planktonic and the biofilm modes of growth [ 31].
We suggest that the plasma membrane-to-ER metabolic shift was in fact the reason for the emergence of the endomembrane system.
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We next examined if the miR-155 mediated metabolic shift is also valid in human cancer.
Understanding how cancer cells drive such metabolic shift is crucial to identify potential targets for cancer therapeutics.
This metabolic shift is thought to be associated with lactic acidosis, organ dysfunction and poor clinical outcomes.
Increased glycolysis has been consistently observed in cancer cells [28], [29], but whether this metabolic shift is a consequence or cause of cancer remains controversial [30].
This metabolic shift is known as aerobic glycolysis, or the Warburg effect.
Furthermore, the metabolic shift is reflected in many sustaining pathways supporting the results.
This metabolic shift is often called the Warburg effect (or Warburg hypothesis).
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