# Consequences of Glucose Enriched Diet on Oncologic Patients
### Role of Sugar in Cancer Metabolism
#### 1.2.1 Sugars in the Diet and Cancer Risk
In this study of American adults [28], the conclusions revealed that a larger intake of sugary beverages is implicated in an enhanced risk of adiposity-related malignancies, among those who shown an excessive central adiposity. Prostate cancer risk was observed to be increased among individuals who consumed more than seven servings of fruit juices per week (more than one serving per day) [28]. In a context where the WHO questioned the level of evidence of scientific data supporting the implementation of a tax on sugary drinks, the outcomes of another observational work with a total of 101,257 participants based on a huge prospective cohort suggested that high consumption of sugary beverages is linked to an increased risk of breast cancer and general cancer [29]. Notably, in this analysis, 100% fruit juices were connected to an increased risk of cancer in general. If these results were replicated in more large-scale prospective studies and supported by mechanistic experimental data, along with the relevant place that sugary drinks have in Western countries' diet, in addition to their well-established impact on cardio metabolic consequences, these drinks may represent a modifiable risk factor for cancer prevention. In contrast, this study revealed no association between drinking artificially sweetened beverages and an increased risk of cancer. These findings held up following a number of sensitivity studies [29]. Adaptation of Cells to a Lack of Glucose  
When challenged by energy stress or glucose deprivation, cells limit protein production and proliferation by activating p53 and AMPK and by inactivating mTOR. These pathways also promote alternate methods to obtain energy. One of those energy reservoirs is fatty acids. In reaction to glucose scarcity, AMPK modifies fatty acid synthesis and stimulates their oxidation. According to various investigations, glioblastoma cells are protected from glucose deprivation when fatty acid oxidation takes place [26; 30]. Glioblastoma cells have been found to utilize glutamine when glucose is low, and if glutamine metabolism is disrupted, the cells are unable to survive without glucose. Therefore, cells employ fatty acids and amino acids to try to maintain homeostatic functions and energy levels when glucose is not available [26]. A conserved reaction to a dearth of nutrition and oxygen is autophagy. It is believed that low glucose levels activates autophagy, and in apoptosis-deficient cells subjected to hypoxia and glucose deprivation, autophagy is important for maintaining cell life [26; 31]. Sensitivity of oncogenes to glucose restriction  
Proliferating cells react to the absence of glucose by actively pushing cell cycle arrest as well as blocking biosynthetic pathways. Still, tumor cells typically demonstrate hyperactivation of pathways associated with alterations in cell cycle inhibitors and proliferation. This makes the cells hypersensitive to glucose deprivation, as the proliferation of the cells are enhanced, but they lack the necessary building blocks for this purpose. Since they are unable to inhibit anabolism in this scenario, cells undergo energy stress and eventually die [26]. A substantial majority of tumor cells lack LKB1, which is the most critical kinase linked with AMPK activation. Because cells missing LKB1 do not respond properly to energy stress, they are hypersensitive to energy-depleting agents. Downstream of AMPK, glucose shortage supports the activation of p27 and p53, which induce autophagy and support cell cycle arrest, which contribute to their survival effects in the absence of glucose [26; 32]. Bcl-2 antiapoptotic proteins and glucose deprivation  
Bcl-2 is the prototype member of a family of proteins that contain at least one Bcl-2 (BH) region of homology.