Abstract
Obesity is associated with a wide range of chronic diseases, including cancer. It has been noted that the integration of metabolic mechanisms in obese patients may predispose them to suffer from cancer incidence and its progression. Thus, a better understanding of metabolic alterations in obesity, along with the development of feasible therapeutic approaches for intervention, are theoretically relevant to the prevention and treatment of cancer malignancy. Using a syngeneic tumor model involving Lewis Lung Carcinoma (LLC) cells and C57BL/6 mice fed with a high fat diet, obesity was found to be associated with dysregulated glucose and glutamine metabolism, inflammation, along with platelet activation and the promotion of tumor growth. Tumor-bearing lowered glucose levels while moderately increasing inflammation, platelet activation, and glutamine levels. The antiplatelet drug aspirin, mitigated tumor growth in obese mice, paralleled by a decrease in systemic glucose, insulin, inflammation, platelet activation, glutamine and tumor expression of cell proliferation, aerobic glycolysis, glutaminolysis, platelets, and leukocyte molecules. The anti- and pro-cell proliferation, aerobic glycolysis, and glutaminolysis effects of aspirin and glutamine were further demonstrated in a LLC cell study. Although there remains limitations to our experiments, glucose and glutamine metabolism are proposed targets for the anticancer effects of aspirin.
Highlights
Obesity is a global concern, which brings upon major health problems
Using a syngeneic tumor model with Lewis Lung Carcinoma (LLC) cells and C57BL/6 mice, we demonstrated that obese mice showed tumor model with LLC cells and C57BL/6 mice, we demonstrated that obese mice showed signs of hyperglycemia, hyperinsulinemia, insulin resistance, hyperleptinemia, low-grade systemic signs of hyperglycemia, hyperinsulinemia, insulin resistance, hyperleptinemia, low-grade systemic inflammation, platelet activation, glutamine elevation, and augmented tumor growth
Glucose and glutamine metabolism appear to have a role in obesity-driven cancer malignancy, and represent targets of aspirin regarding anticancer
Summary
Obesity is a global concern, which brings upon major health problems. Beyond its immediate and obvious health significance, obesity is associated with an increased risk and poorer outcome for many chronic diseases, including cancer [1]. Hyperglycemia, hyperinsulinemia, and chronic, low-grade inflammation are hallmarks of obesity. It has been postulated that hyperglycemia, hyperinsulinemia, adipokines, and cytokines in obese subjects provide abundant nutrients and growth factors for cancer cells, resulting in the establishment of an appropriate niche for tumor progression and malignancy [1,2,3]. Obesity may integrate several metabolic mechanisms to predispose suffering from cancer incidence and progression. A better understanding of metabolic alterations surrounding obesity, along with the development of feasible therapeutic approaches for intervention are theoretically relevant to the treatment and prevention of cancer malignancy
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