Consequences of Glucose Enriched Diet on Oncologic Patients

Abstract

Malignant tumors demonstrate increased rates of glucose utilization and uptake. Therefore, clinical trials are being used to evaluate a variety of inhibitors of glycolytic metabolism. Antiglycolytic drugs have been proven to promote chemotherapy and radio-induced cell death. Glucose influences the levels and activation of pro-apoptotic BH3-only proteins, such as Puma, Bad, Noxa, and Bim, and the family of anti-apoptotic proteins Bcl-2; synergistic effects are probably the result of the regulation of the apoptotic machinery. Antiglycolytic medicines and glucose deprivation induce tumor cell death by caspase-8-mediated or mitochondrial apoptosis or even necrosis. The last is known to activate the effector caspases, principally through the cleavage of the Bcl-2 family member Bid and the consequent activation of the mitochondrial pathway. Modifications to the host’s diet can modify the availability of nutrients in the tumor microenvironment, which could offer a feasible technique to restrict growth. Dietary alterations can reduce particular nutritional requirements of the tumor that target the metabolic vulnerabilities or boost the cytotoxicity of anticancer medications. According to recent studies, increasing the amount of key minerals in the diet can affect how well cancer therapies can function. The research reveals that the eating habits and nutritional state of a patient should be regarded during cancer research and therapy.

Keywords

• apoptosis
• Bcl2 proteins
• cancer
• glucose
• nutrition
• Warburg effect