據美國《每日科學》10月31日報道，瑞典歌德堡大學日前研究發現，人們減少攝取卡路裏不僅有助於延緩衰老，還有利於推遲糖尿病、癌症等老年病的患病期，且越早減少卡路裏的攝入量效果越明顯。
該研究的負責人歌德堡大學細胞分子生物學專家米卡埃爾·莫林介紹說：“研究表明，人體內有一種酶是延緩人體老化的關鍵因素，它叫氧化還原酶 （peroxiredoxin），減少卡路裏的攝取量能夠有效保持這種酶的活性。不僅如此，這種酶對人體還有個至關重要的作用，它可以有效保護我們體內的 基因物質。”
雖然研究人員目前尚不能解釋這種“延年益壽大法”的確切原理，但就目前掌握的研究結果來開，具備活性的過氧還原酶可以降 解人體細胞內的有害物質過氧化氫，而這種酶隻有當人體的卡路裏攝入量在得到一定限製時才會很好的發揮功效。隨著人們年齡的增長，體內的過氧還原酶會逐漸遭 到破壞，失去活性，但有一種酶可以對其進行修複，它就是Srx1，減少卡路裏的攝取量會促使人體增加Srx1的產量。
據悉，研究者在實驗中以猴子為實驗對象，通過逐漸降低糖和蛋白的攝入量，保持維生素和礦物質的攝入量，這些猴子的壽命明顯延長了數年。研究者隨即在魚類、齧齒類、昆蟲、菌類等多個物種上進行了相同實驗，都取得良好效果。
研究人員目前正在檢驗過氧還原酶是否也可以減少或延緩人類的神經類疾病，因為該種酶同時也對人類體內的蛋白質有保護作用，其保護人體蛋白質的過程又與一些神經係統類的老年病息息相關。
By consuming fewer calories, aging can be slowed down and the development of age-related diseases such as cancer and type 2 diabetes can be delayed. The earlier calorie intake is reduced, the greater the effect. Researchers at the University of Gothenburg have now identified one of the enzymes that hold the key to the aging process…
“We are able to show that caloric restriction slows down aging by preventing an enzyme, peroxiredoxin, from being inactivated. This enzyme is also extremely important in counteracting damage to our genetic material,” says Mikael Molin of the Department of Cell and Molecular Biology.
By gradually reducing the intake of sugar and proteins, without reducing vitamins and minerals, researchers have previously shown that monkeys can live several years longer than expected. The method has also been tested on everything from fishes and rats to fungi, flies and yeasts with favourable results. Caloric restriction also has favourable effects on our health and delays the development of age-related diseases. Despite this, researchers in the field have found it difficult to explain exactly how caloric restriction produces these favourable effects.
Using yeast cells as a model, the research team at the University of Gothenburg has successfully identified one of the enzymes required. They are able to show that active peroxiredoxin 1, Prx1, an enzyme that breaks down harmful hydrogen peroxide in the cells, is required for caloric restriction to work effectively.
The results, which have been published in the journal Molecular Cell, show that Prx1 is damaged during aging and loses its activity. Caloric restriction counteracts this by increasing the production of another enzyme, Srx1, which repairs Prx1. Interestingly, the study also shows that aging can be delayed without caloric restriction by only increasing the quantity of Srx1 in the cell. Repair of the peroxiredoxin Prx1 consequently emerges as a key process in aging.
“Impaired Prx1 function leads to various types of genetic defects and cancer. Conversely, we can now speculate whether increased repair of Prx1 during aging can counteract, or at least delay, the development of cancer.”
Peroxiredoxins have also been shown to be capable of preventing proteins from being damaged and aggregating, a process that has been linked to several age-related disorders affecting the nervous system, such as Alzheimer’s and Parkinson’s. The researchers are accordingly also considering whether stimulation of Prx1 can reduce and delay such disease processes.
http://www.sciencedaily.com/releases/2011/10/111031215938.htm
