營養與代謝雜誌(Nutrition & Metabolism) 2011, 8:75
Rainer J Klement 1* and Ulrike Kämmerer 2
1Department of Radiation Oncology, University hospital of Würzburg, D-
97080 Würzburg, Germany. 2 Department of Obstetrics and Gynaecology,「
University hospital of Würzburg, D-97080 Würzburg, Germany.

在過去幾年中,累積的證據已經顯示通過系統地減少碳水化合物(CHOS)飲食量,能抑制或至少延遲腫瘤出現,以及讓已經存在腫瘤細胞的擴散減慢。

這種假設乃因現代的慢性疾病,如新陳代謝症候群與發生或死於癌症風險之間的關聯性而得到支持。
CHOS或葡萄糖,甚至最終也會被消化的更複雜碳水化合物,會直接和間接影響腫瘤細胞的增殖:
第一,與正常細胞不同,大多數惡性腫瘤細胞因為線粒體功能障礙(mitochondrial dysfunction)而不能夠代謝脂肪酸(fatty acid)或酮體(Ketone bodies),因此需依賴於血中穩定的葡萄糖供應作為它們的能量和腫瘤生長需求的來源。

第二,長期攝入含CHO豐富的西方化飲食,導致胰島素和胰島素生長因子(IGF)-1上升,而經由胰島素/ IGF-1信號通路,會直接促進腫瘤細胞增殖。

第三,體外研究顯示當胰島素和血糖低時,酮體升高會對不同的惡性細胞增殖產生負面影響,而且腫瘤細胞的代謝需求無法利用酮體進行。另外眾多的老鼠實驗模式顯示非常低的CHO生酮飲食具有抗腫瘤的特性。
此外,許多癌症患者因胰島素抗性(insulin resistance)伴隨葡萄糖代謝改變,卻因增加蛋白質和脂肪的攝入量而受益。

在本篇文獻中,我們針對低CHO的飲食對癌症的預防和治療可能有益影響進行回顧性探討。其重點將放在胰島素和IGF-1在腫瘤信號傳導中的作用,以及癌症患者飲食需求之改變。

評論: 此文獻針對低糖飲食與癌症的關係做一完整回顧性的探討(參考文獻162篇),值得參考,先翻譯摘要的部分,有興趣的同工可自行下載完整原文參考。

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

Nutrition & Metabolism 2011, 8:75
Rainer J Klement 1* and Ulrike Kämmerer 2

Abstract
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 antitumorigenic 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.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267662/pdf/1743-7075-8-75.pdf

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