紅肉與癌症:還有未知機轉?


  【24drs.com】一直有文獻提到長期攝取紅肉與某些癌症風險較高有關,特別是大腸直腸癌。
  
  現在,加州大學聖地牙哥分校的研究者,證明紅肉中的某種特殊糖類會促進發炎與癌症病程。不過,他們在線上發表於12月29日美國國家科學院院刊的文章中也指出,他們進行的是老鼠研究,結果還無法應用於人類。
  
  研究聚焦在稱為「非人類唾液酸N-羥基乙醯神經胺酸(Neu5Gc)」的一種糖類,自然存在於人類以外的多數哺乳類動物,它可見於多種肉類,尤其是人類經常食用的牛肉、豬肉、羊肉。
  
  這篇研究中,研究者假設吃紅肉會導致發炎,如果人類身體免疫系統不斷產生抗體,對抗吃到的動物Neu5Gc這個外來分子的話。
  
  為了測試這個假設,研究團隊需要一個類似人類的動物模式,也就是要像人類一樣沒有Neu5Gc。他們運用基因工程讓老鼠缺乏Neu5Gc,藉以模擬人類產生抗體的情況。
  
  當這些基因改造老鼠被餵食Neu5Gc時,牠們發生全身性發炎,肝臟的自發性腫瘤形成增加5倍、Neu5Gc累積在腫瘤中。研究者解釋,這類老鼠容易發生肝腫瘤,因此可以解釋為何該處發現惡性腫瘤。
  
  第一作者、美國聖地牙哥Moores癌症中心的Ajit Varki醫師在新聞聲明稿中表示,這是首度直接顯示模擬人類的實際狀況─餵食非人類的Neu5Gc且誘導對抗Neu5Gc之抗體─增加了老鼠的自發性癌症。
  
  他指出,迄今,我們有關Neu5Gc與癌症關聯的證據,都是旁證或者間接得自一定程度人為之實驗裝置的預測。
  
  Varki醫師也表示,在人類的最終證明會更難獲得。 不過,他也表示,新發現可以幫助解釋攝取紅肉和其他受慢性發炎而惡化的疾病,如粥狀動脈硬化與第二型糖尿病之潛在關聯。
  
  新研究為攝取紅肉與癌症風險提供更實質的文獻。
  
  不過,這兩者的關聯還未被明確證實,多方面的證據都還顯薄弱。
  
  資料來源:http://www.24drs.com/professional/list/content.asp?x_idno=7149&x_classno=0&x_chkdelpoint=Y
  

Red Meat and Cancer: Has a Mechanism Been Uncovered?

By Nick Mulcahy
Medscape Medical News

The long-term consumption of red meat has repeatedly been associated with a higher risk for certain cancers in humans, particularly colorectal cancer.

Now researchers at the University of California (UC), San Diego, have evidence that a specific type of sugar found in red meat may promote inflammation and cancer progression.

However, their study is in mice, and their results may be hard to demonstrate in humans, they acknowledge in an article published online December 29 in the Proceedings of the National Academy of Sciences.

The focus of the research is a sugar known as nonhuman sialic acid N-glycolylneuraminic acid (Neu5Gc), which is naturally found in most mammals but not in humans. It occurs in varieties of meat, especially beef, pork, and lamb, that humans often consume.

In this study, the researchers hypothesized that eating red meat could lead to inflammation ─ if the human body's immune system is constantly generating antibodies against consumed animal Neu5Gc, a foreign molecule.

To test this hypothesis, the team needed an animal model that was similar to humans insofar as the animal would, like humans, not have Neu5Gc itself.

They managed to create that by genetically engineering mice that lacked Neu5Gc and thus produced antibodies against it, mimicking the situation in humans.

When these genetically engineered mice were fed Neu5Gc, they developed systemic inflammation, with a fivefold increase in spontaneous tumor formation in the liver and Neu5Gc accumulation in the tumors. The researchers explained that such mice are prone to liver tumors, which could account for why the malignancies showed up there.

"This is the first time we have directly shown that mimicking the exact situation in humans ─ feeding nonhuman Neu5Gc and inducing anti-Neu5Gc antibodies ─ increases spontaneous cancers in mice," said lead author Ajit Varki, MD, of the UC San Diego Moores Cancer Center, in a press statement.

"Until now, all of our evidence linking Neu5Gc to cancer was circumstantial or indirectly predicted from somewhat artificial experimental setups," he added.

"The final proof in humans will be much harder to come by," Dr Varki also said.

However, he also said that the new findings may help explain potential connections between red meat consumption and other diseases exacerbated by chronic inflammation, such as atherosclerosis and type 2 diabetes.

The new research adds to a substantial body of literature about red meat consumption and cancer risk.

However, the association between the two has never been definitively proven. The weaknesses of the evidence are manifold, as noted in an article published in 2013 by Medscape Medical News.

The research was funded by the Ellison Medical Foundation, the National Cancer Institute, a Samuel and Ruth Engelberg fellowship from the Cancer Research Institute, and a Swiss National Science Foundation fellowship. Dr Ajit Varki and a colleague are cofounders and have equity interest in SiaMab Therapeutics, Inc, a biotech company with an interest in Neu5Gc and anti-Neu5Gc antibodies.

Proc Natl Acad Sci. Published online December 29, 2014.

    
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