Nupur Rani Agarwal,1* Nancy Maurya2*Proceedings of the Nature Research Society, 2018, Volume 2, Article Number 02009Published Online: 26 June 2018 (Review)DOI:10.11605/j.pnrs.201802009
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Cancer is a metabolic disease. Their typical characteristic is high consumption of glucose as these cells mostly have defective mitochondria. They primarily derive energy through aerobic glycolysis even in presence of abundant oxygen. Cancer cells thus are heavily dependent on ample and continuous availability of glucose for growth, proliferation and invasion. These cells adopt various strategies to satisfy their high demand for sugar which includes modification in signalling pathways and abnormally high expression of glucose transporters. Glucose uptake is favoured by alteration in PI3K-Akt-mTOR pathway. High glucose condition creates conducive environment for cancer cells to flourish. The H+ ion secreted as by-product of glycolysis helps in invasion and metastasis. Other by products of glycolysis which includes ATP, NADP and NADPH also aids in growth of cancer cells. Glucose restriction puts break on speedy multiplying tumor cells as unlike normal cells of the body they are unable to metabolize any other source of fuel. Lower glucose level induces changes in level of cleaved caspase 3, Bcl-2, p53 and p21 which prompts senescence and apoptosis in rapidly proliferating tumor cells. Various strategies can be employed to cut down glucose accessibility to cancer cells such as inhibition of glucose transporters, adoption of keto diet. Combining glucose restriction with either chemo or radiotherapy increases their effectiveness; lower CHO levels also provide protection to normal healthy cells of the body against toxic effect of anti-carcinogens. Carbohydrate restriction is a non- toxic, easily impeccable, economical and safe tactic which may be utilized as weapon in war against cancer.
Citation Information: Nupur Rani Agarwal, Nancy Maura, Low Sugar Diet: A New Tool in War Against Tumorigenesis, Proceedings of the Nature Research Society, 2018, 2, 02009. doi: 10.11605/j.pnrs.201802009
Received: 26 April 2018, Accepted: 25 June 2018, Published Online: 26 June 2018