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Is there a role for carbohydrate restriction in the treatment and prevention of cancer?

机译:限制碳水化合物在癌症的治疗和预防中有作用吗?

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Over the last years, evidence has accumulated suggesting that by systematically reducing the amount of dietary carbohydrates (CHOs) one could suppress, or at least delay, the emergence of cancer, and that proliferation of already existing tumor cells could be slowed down. This hypothesis is supported by the association between modern chronic diseases like the metabolic syndrome and the risk of developing or dying from cancer. CHOs or glucose, to which more complex carbohydrates are ultimately digested, can have direct and indirect effects on tumor cell proliferation: first, contrary to normal cells, most malignant cells depend on steady glucose availability in the blood for their energy and biomass generating demands and are not able to metabolize significant amounts of fatty acids or ketone bodies due to mitochondrial dysfunction. Second, high insulin and insulin-like growth factor (IGF)-1 levels resulting from chronic ingestion of CHO-rich Western diet meals, can directly promote tumor cell proliferation via the insulin/IGF1 signaling pathway. Third, ketone bodies that are elevated when insulin and blood glucose levels are low, have been found to negatively affect proliferation of different malignant cells in vitro or not to be usable by tumor cells for metabolic demands, and a multitude of mouse models have shown anti-tumorigenic properties of very low CHO ketogenic diets. In addition, many cancer patients exhibit an altered glucose metabolism characterized by insulin resistance and may profit from an increased protein and fat intake. In this review, we address the possible beneficial effects of low CHO diets on cancer prevention and treatment. Emphasis will be placed on the role of insulin and IGF1 signaling in tumorigenesis as well as altered dietary needs of cancer patients.
机译:在过去的几年中,已有证据表明,通过系统地减少饮食中的碳水化合物(CHO)的量,可以抑制或至少延迟癌症的出现,并且可以减慢已经存在的肿瘤细胞的增殖。这一假设得到了现代慢性疾病(如代谢综合症)与癌症发生或死亡风险的关联的支持。最终会被更复杂的碳水化合物消化的CHOs或葡萄糖,会对肿瘤细胞的增殖产生直接和间接的影响:首先,与正常细胞相反,大多数恶性细胞对血液中能量和生物质产生的需求依赖于稳定的葡萄糖可用性。由于线粒体功能障碍,它们不能代谢大量的脂肪酸或酮体。第二,长期摄入富含CHO的西方饮食所产生的高胰岛素和胰岛素样生长因子(IGF)-1水平可以通过胰岛素/ IGF1信号通路直接促进肿瘤细胞增殖。第三,已发现当胰岛素和血糖水平低时酮体升高,在体外对不同恶性细胞的增殖产生负面影响,或不能被肿瘤细胞用于代谢需求,并且许多小鼠模型显示抗极低的CHO生酮饮食的致瘤特性。另外,许多癌症患者表现出以胰岛素抵抗为特征的葡萄糖代谢改变,并可能因蛋白质和脂肪摄入增加而受益。在这篇综述中,我们探讨了低CHO饮食对癌症预防和治疗的可能有益作用。重点将放在胰岛素和IGF1信号传导在肿瘤发生以及癌症患者饮食需求改变中的作用。

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