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2020年癌症研究:生酮饮食对脑肿瘤代谢的影响-莫塔j -佛罗里达大学

摘要

目的:在一名肿瘤患者中建立饮食诱导的酮症，以确定生酮状态是否会降低某些肿瘤的葡萄糖可用性，从而可能损害肿瘤代谢，而不会对患者的整体营养状况产生不利影响。简介:人类威胁性神经胶质瘤是一种一贯致命的疾病，在某种程度上，由于目前可获得的药物的限制，包括医疗程序，化疗和放疗。多形性胶质母细胞瘤(GBM)患者的正常生存期为1.5年，而局灶性感觉系统肿瘤是儿科人群中最被广泛认可的恶性肿瘤。正是在这种至关重要的意义上，精神恶性生长患者的新治疗技术得以发展，特别是那些能够在不伤害普通大脑组织的情况下提高现有治疗方案的充分性的技术。我们对这些肿瘤的科学理解的进步促进了临床前和临床初步集中治疗的数量的扩大。虽然这些治疗可能在一定程度上证明是成功的，但这种肿瘤的异质性经常阻止在肿瘤的所有细胞上发现原子的焦点，从而降低了这些药物的可行性。相反，所有肿瘤细胞所共有的一个特征是调节代谢。“代谢重新设计”一词已被用来描述恶性生长细胞中可能发生的代谢变化，而目前已知的致癌基因相关途径与代谢途径交叉并改变代谢途径。KD是一种用于治疗顽固性癫痫的高脂肪、低蛋白质/淀粉饮食(Kim和Rho, 2008;十字架,2013)。 It has been appeared to have neuroprotective impacts and there are presently studies to decide its adequacy for various neurological issue, including epilepsy, Alzheimer's infection, Parkinson's sickness, rest issue, migraine, awful mind injury, amyotrophic sidelong sclerosis, torment and chemical imbalance (Masino and Ruskin, 2013; Gano et al., 2014). The KD expands blood ketones and diminishes blood glucose by mimicking the physiological reaction to fasting, consequently prompting high paces of unsaturated fat oxidation and an expansion in the creation of acetyl coenzyme An (acetyl-CoA). Case report: One pet male with advanced stage brain tumor. Patient was followed as outpatients for 1 year. Ketosis was maintained by consuming a 60% medium chain triglyceride oil-based diet. Some cancers cannot metabolize ketone bodies, due to mitochondrial dysfunction and down-regulation of enzymes necessary for ketone utilization. Tumor glucose metabolism was assessed by RMI, before and following the trial period. As radiation-initiated tumor slaughtering is known to uncover the resistant framework to a more noteworthy decent variety of tumor antigens, it is conceivable that the KD as an adjuvant attempts to enlarge the impact of radiation partially by upgrading invulnerability against GBM. The assortment of impacts seen when glucose in brought down or potentially ketones are expanded recommends this may likewise potentiate different treatments, including more up to date safe and focused on treatments. Results: Within 7 days of initiating the ketogenic diet, blood glucose levels declined to low-normal levels and blood ketones were elevated. Results of RMI indicated a 50% average decrease uptake at the tumor site in subject. The patient exhibited significant clinical improvements in seizures, neurological deficits and new skill development during the treatment. He still continues used the ketogenic diet remaining free of disease progression. Conclusion: While this diet does not replace conventional antineoplastic treatments, these preliminary results suggest a potential for clinical application which merits further research.

莫塔J。

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