# Consequences of Glucose Enriched Diet on Oncologic Patients
### Role of Sugar in Cancer Metabolism
#### 1.2.5 Dietary Changes for Effective Cancer Therapy
A combination of pharmacological and dietary insulin suppression is likely a more effective way to stop tumor growth. After pharmacologically inhibiting PI3K, this strategy was tested in animals, and it was discovered that dietary glucose restriction using a ketogenic diet prevented compensatory insulin secretion and hyperglycemia. The combination approach resulted in decreased pro-oncogenic signaling through mTOR, improved tumor suppression, and enhanced survival of tumor-bearing mice in multiple cancer types. These findings are highly promising for individuals treated with PI3K inhibitors [70]. Although most cancers develop efficiently in the presence of excess glucose and all tumors feed on glucose, some tumors progress more rapidly when fat is supplied for energy. In these rare instances, patients will gain from diets in which carbohydrates serve as the primary energy source. For that reason, before making any suggestions to the patients, it is vital to finish the preclinical study of the results of the changes in the diet's energy source and investigate the metabolic preferences of each tumor type. The potential advantages of a ketogenic diet for cancer patients have been investigated in numerous clinical studies. These trials were performed utilizing a small number of participating patients, making it impossible to infer whether the ketogenic diet has important benefits. In addition, the lack of a standardized procedure for this diet, as well as the considerable diversity in patients' adherence to the diet, makes it impossible to compare their results. Nevertheless, a handful of these studies have shown positive data that dietary sugar restriction with a ketogenic diet is viable for persons with various forms of advanced cancer is safe and produces superior results in cancer patients. Although several of these trials did not demonstrate that glucose withdrawal significantly suppressed tumor growth, they laid the framework for future research that should focus on meticulous compliance monitoring and a standardized regimen for a ketogenic diet. Evaluation of the ketogenic diet's efficacy in the earliest stagesof cancer progression is also anticipated to generate superior results. Moreover, limiting glucose intake, managing insulin secretion and blood glucose levels, and assisting patients in maintaining low-carbohydrate diets are likely to improve cancer patients' survival [70]. In the Western diet, fructose is extremely common. In light of the emerging understanding regarding the fate of fructose absorbed through diet and its role in cancer progression, cancer patients' fructose intake must be carefully evaluated. Only epidemiological studies had previously demonstrated a negative pro-tumorigenic effect of fructose consumption, but this is now evident. Tumor cells can use fructose as an energy source, and many cancers import massive amounts of fructose by upregulating the fructose transporter GLUT5. The inhibitory effect of GLUT5 silencing on the growth of cancer in animal and in vitro models highlights the dependence of malignancies on fructose as an energy source. Although fructose is processed and absorbed mostly via the intestine, it gets spilled to the liver if it is ingested in large quantities, thus overwhelming the intestinal capacity for fructose absorption. When fructose reaches the liver, it leads to obesity, type 2 diabetes, de novo lipid synthesis, fatty liver, and increased blood triglyceride production. In an Apc mice model, even modest chronic fructose consumption (equivalent to one can of soda per day) has been found to increase the risk of colon cancer [74]. The discovery that this low amount is sufficient to induce fatty acid production, tumor growth, and glycolysis in intestinal tumors contradicts the commonly held belief that, at least in the intestine, only a considerable excess of fructose can cause cancer [70; 74].