摘要
临床前和临床研究已经调查了失调代谢在肿瘤发生和进展的可持续性中的作用。在几种类型癌症中遇到的最熟悉的代谢改变之一是糖酵解的上调,其也保持在正常氧压力(有氧糖酵解,Warburg效应)的条件下,而氧化磷酸化明显降低。结果是癌细胞将大部分进入的葡萄糖转化成乳酸。尽管转化速度变快,但通过糖酵解产生的三磷酸腺苷(ATP)比氧化磷酸化消耗的每单位葡萄糖产生的ATP效率更低,结果是,与正常对照物相比,肿瘤细胞需要异常较高的葡萄糖比例。新的证据表明,其他代谢底物如谷氨酰胺也可能在癌症代谢中起重要作用。生酮饮食(KD)用低至中等量的蛋白质和大量的单不饱和和多不饱和脂肪代替非淀粉植物碳水化合物。 KD的理由是有效的,因为它降低碳水化合物摄取可能导致癌细胞饥饿和凋亡,并且同时增加正常细胞中可用于能量产生的酮体的水平,但不增加据称下调的癌细胞氧化磷酸化。因此,几位作者推测将KD评估为治疗癌症的新方法的可能性。在这次审查中,我们将评估支持使用这种消化方案的数据及其对肿瘤发展和进展的影响。
关键词: 癌症,生酮饮食,低碳水化合物饮食,碳水化合物限制,有氧糖酵解,热量限制。
Current Medicinal Chemistry
Title:Ketogenic Diet and Other Dietary Intervention Strategies in the Treatment of Cancer
Volume: 24 Issue: 12
关键词: 癌症,生酮饮食,低碳水化合物饮食,碳水化合物限制,有氧糖酵解,热量限制。
摘要: Pre-clinical and clinical studies have investigated the role of a dysregulated metabolism in the sustainability of tumor initiation and progression. One of the most familiar metabolic alterations encountered in several types of cancers is the upregulation of glycolysis, which is also maintained in conditions of normal oxygen tension (aerobic glycolysis, Warburg effect) while oxidative phosphorylation is apparently reduced. As a result, cancer cells convert most incoming glucose to lactate. Although more rapid, adenosine triphosphate (ATP) production by glycolysis is less efficient in terms of ATP generated per unit of glucose consumed than oxidative phosphorylation. The consequence is that tumor cells require an abnormally higher rate of glucose compared to the normal counterpart. New evidence shows that other metabolic substrates such as glutamine may also have an important role in cancer metabolism. Ketogenic diet (KD) replaces all but non-starchy vegetable carbohydrates with low to moderate amounts of proteins and high amounts of monounsaturated and polyunsaturated fats. The rationale of KD is valid both because it lowers carbohydrate uptake possibly leading to cancer cell starvation and apoptosis and, at the same time, increases the levels of ketone bodies available for energy production in normal cells but not in cancer cells which have an allegedly downregulated oxidative phosphorylation. For this reason, several authors speculate on the possibility to evaluate KD as a novel approach in the treatment of cancer. In this review we will assess the data supporting the use of such alimentary regimen and its impact on tumor development and progression.
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Cite this article as:
Ketogenic Diet and Other Dietary Intervention Strategies in the Treatment of Cancer, Current Medicinal Chemistry 2017; 24 (12) . https://dx.doi.org/10.2174/0929867324666170116122915
DOI https://dx.doi.org/10.2174/0929867324666170116122915 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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