科學家長期以來科學家們一直被這個問題困擾：怎樣能夠通過飲食限制,，或者相反,，過多消耗能量,，來避免衰老和疾病,？西奈山醫(yī)學院的研究者正在試圖解決這個問題,。
西奈山醫(yī)學院神經(jīng)科學和老年病學與緩解醫(yī)學的教授Charles Mobbs博士領(lǐng)導了一項研究發(fā)現(xiàn)一個分子可決定某些參數(shù)，就像低熱量飲食可以延緩一些年齡相關(guān)疾病如早老性癡呆的發(fā)展,，也可以延緩衰老過程,，結(jié)果發(fā)表在11月17日出版的《公共圖書館·生物學》雜志上。
他們發(fā)現(xiàn)一個分子,，可以決定某些參數(shù),，就像低熱量飲食可以延緩一些年齡相關(guān)疾病如早老性癡呆的發(fā)展，也可以延緩衰老過程,。如何限制飲食,，脂肪、蛋白質(zhì)或者碳水化合物哪些被減掉,，好像并不重要,。Mobbs博士說：“這可能不是卡路里計算或者減掉特殊營養(yǎng)的問題，而是減少飲食如何影響葡萄糖代謝的問題,，糖代謝會導致氧化壓力,。高卡路里飲食可能會通過加重氧化壓力，使衰老相關(guān)疾病加重,。”
飲食限制會誘導一種叫做CREB結(jié)合蛋白（CBP）的轉(zhuǎn)錄因子,，后者控制調(diào)節(jié)細胞功能基因的活性。研發(fā)能夠模擬CBP保護作用的藥物（就像限制飲食引起的作用）,，科學家們可能會延長人類壽命,，降低衰老相關(guān)疾病的發(fā)病率。
Mobbs博士說：“我們發(fā)現(xiàn)CBP可以預測壽命,，在決定哺乳動物壽命差異的因素中權(quán)重占80%,。找到正向平衡是關(guān)鍵，只要限制10%就會使壽命延長一些,，而限制80%卻會因為饑餓導致壽命縮短,。”
工作組發(fā)現(xiàn)一個最佳的飲食限制，估計相當于減少哺乳動物卡路里攝入量的30%,，就會延緩類似早老性癡呆等年齡相關(guān)病理狀態(tài),，將壽命延長50%,。（生物谷Bioon.com）
生物谷推薦原始出處：
PLoS Biol 7(11): e1000245. doi:10.1371/journal.pbio.1000245
Role of CBP and SATB-1 in Aging, Dietary Restriction, and Insulin-Like Signaling
Minhua Zhang1, Michal Poplawski1, Kelvin Yen1, Hui Cheng1, Erik Bloss1, Xiao Zhu1, Harshil Patel1, Charles V. Mobbs1,2*
1 Department of Neuroscience, Mount Sinai School of Medicine, New York, New York, United States of America, 2 Department of Geriatrics, Mount Sinai School of Medicine, New York, New York, United States of America
How dietary restriction (DR) increases lifespan and decreases disease burden are questions of major interest in biomedical research. Here we report that hypothalamic expression of CREB-binding protein (CBP) and CBP-binding partner Special AT-rich sequence binding protein 1 (SATB-1) is highly correlated with lifespan across five strains of mice, and expression of these genes decreases with age and diabetes in mice. Furthermore, in Caenorhabditis elegans, cbp-1 is induced by bacterial dilution DR (bDR) and the daf-2 mutation, and cbp-1 RNAi specifically in adults completely blocks lifespan extension by three distinct protocols of DR, partially blocks lifespan extension by the daf-2 mutation but not of cold, and blocks delay of other age-related pathologies by bDR. Inhibiting the C. elegans ortholog of SATB-1 and CBP-binding partners daf-16 and hsf-1 also attenuates lifespan extension by bDR, but not other protocols of DR. In a transgenic Aβ42 model of Alzheimer's disease, cbp-1 RNAi prevents protective effects of bDR and accelerates Aβ42-related pathology. Furthermore, consistent with the function of CBP as a histone acetyltransferase, drugs that enhance histone acetylation increase lifespan and reduce Aβ42-related pathology, protective effects completely blocked by cbp-1 RNAi. Other factors implicated in lifespan extension are also CBP-binding partners, suggesting that CBP constitutes a common factor in the modulation of lifespan and disease burden by DR and the insulin/IGF1 signaling pathway.
