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In our previous article (1), we presented a unifying principle in the hypotheses of Pasteur, Warburg, and Crabtree that “an inverse relation exists between glucose uptake and respiration.” Warburg’s hypothesis laid emphasis on glucose metabolism and damaged respiration (mitochondria) for growth of cells in cancer (2). Pasteur recognized that yeast can grow only if ammonium tartrate (nitrogen source) is available, whether oxygen is available or not (3) and ammonium is transformed into a “complex albuminoid” (protein) material. Growth is faster in the presence of oxygen and for producing one unit of mass, yeast requires only 1/15th of glucose when compared to that in the absence of oxygen (4–10 parts as against 60–80 parts). Since the ratio of ATP produced per one glucose molecule in glycolysis/oxidative phosphorylation (OXPHOS) is 1:15, the energy consumed per unit of growth of yeast remains same (60X1 and 4X15 ATP). We call this: “the Pasteur’s dictum,” which is different from the “Pasteur effect” introduced by Warburg. Lagunas et al. (4) in early 80s reported that Pasteur effect is observed only in resting cells in the absence of nitrogen, but not in growing cells. Warburg’s hypothesis relies on energetics of glucose metabolism and damaged respiration but ignores Pasteur’s demonstration of nitrogen as the primary requirement for triggering growth. It also ignores the anabolic functions of mitochondria (5, 6) and the role of glutamine, another key nutrient avidly consumed by actively proliferating cells (7, 8). We present in this article, a hypothesis that activation of complexes of mechanistic target of rapamycin (mTORC1 and C2) by amino acids (nitrogen source) is the molecular explanation of the “Pasteur’s dictum.” Amino acids activate both mTORC1 and C2 independent of insulin or growth factor signaling (IIS). Amino acids are also required for activation of mTORC1 in IIS dependent pathway.

The Pasteurâ€™s Dictum: Nitrogen Promotes Growth and Oxygen Reduces the Need for Sugar