多年來，飲食健康總是一個沒有定論的話題，各路專家們（注意，Ta們都是正規的，在高影響因子的雜誌發表論文的專家）各說不一。什麽 Plant based diet, Ketogenic diet........把我們這些外行人弄的昏頭轉向。
一直認為，低碳飲食是抗癌的方向。有很多論文了。大家自己去看吧。但最近，中國的研究者們又發現了相反的實驗數據：低碳飲食可能會促進癌症的肺轉移！媽呀！這一下大家更昏頭轉向了。
這是一篇基礎醫學論文，發表在今年的Cell 雜誌上（很高影響因子的雜誌）。我隻是一個醫者，大概明白論文的意思（勉強用Google translate 譯成中文，並修飾了一下）。用心的讀者可以直接讀原文（如下）。
大概意思是，低碳（剝奪葡萄糖）飲食會通過一係列反應（亞細胞結構，酶，細胞信號），影響到巨噬細胞，最後導致自然殺傷細胞（NK）的耗竭（NK 細胞是抗腫瘤細胞）， 從而建立了腫瘤轉移的微環境。
文章最後說：低碳抗癌的探究/方向，既提供了抗腫瘤治療的思路，也提供了腫瘤轉移危險的思路（雙刃劍）！ 朋友們，自己選擇吧！
摘要的中文翻譯
葡萄糖代謝作為靶向
英文摘要
Targeting glucose metabolism has emerged as a promising strategy for inhibiting tumor growth. However, we herein uncover an unexpected paradox: while glucose deprivation through a low-carbohydrate diet or impaired in situ metabolism suppresses primary tumor growth, it simultaneously promotes lung metastasis by depleting natural killer (NK) cells via lung macrophages. Mechanistically, glucose deprivation induces endoplasmic reticulum (ER) stress, activating HMG-CoA reductase degradation protein 1 (HRD1) to catalyze K63-linked ubiquitination of TRAIL, which is then packaged into exosomes via the endosomal sorting complex required for transport (ESCRT) complex. These exosomal TRAIL molecules polarize PVR+ macrophages, triggering NK cell exhaustion and establishing a pre-metastatic niche. Notably, TIGIT blockade not only prevents metastasis induced by glucose deprivation but also enhances its anti-tumor effects. Clinically, low glucose metabolism correlates with higher 2-year postoperative recurrence across 15 cancer types. Furthermore, plasma exosomal TRAIL outperforms traditional markers, such as α-fetoprotein (AFP) and tumor size, in predicting early postoperative lung metastasis, revealing both the risks and therapeutic potential of targeting glucose metabolism.
下麵是本文的發表的雜誌（Cell）題目，和作者
