科学家长期以来科学家们一直被这个问题困扰：怎样能够通过饮食限制，或者相反，过多消耗能量，来避免衰老和疾病？西奈山医学院的研究者正在试图解决这个问题。
西奈山医学院神经科学和老年病学与缓解医学的教授Charles Mobbs博士领导了一项研究发现一个分子可决定某些参数，就像低热量饮食可以延缓一些年龄相关疾病如早老性痴呆的发展，也可以延缓衰老过程，结果发表在11月17日出版的《公共图书馆·生物学》杂志上。
他们发现一个分子，可以决定某些参数，就像低热量饮食可以延缓一些年龄相关疾病如早老性痴呆的发展，也可以延缓衰老过程。如何限制饮食，脂肪、蛋白质或者碳水化合物哪些被减掉，好像并不重要。Mobbs博士说：“这可能不是卡路里计算或者减掉特殊营养的问题，而是减少饮食如何影响葡萄糖代谢的问题，糖代谢会导致氧化压力。高卡路里饮食可能会通过加重氧化压力，使衰老相关疾病加重。”
饮食限制会诱导一种叫做CREB结合蛋白（CBP）的转录因子，后者控制调节细胞功能基因的活性。研发能够模拟CBP保护作用的药物（就像限制饮食引起的作用），科学家们可能会延长人类寿命，降低衰老相关疾病的发病率。
Mobbs博士说：“我们发现CBP可以预测寿命，在决定哺乳动物寿命差异的因素中权重占80%。找到正向平衡是关键，只要限制10%就会使寿命延长一些，而限制80%却会因为饥饿导致寿命缩短。”
工作组发现一个最佳的饮食限制，估计相当于减少哺乳动物卡路里摄入量的30%，就会延缓类似早老性痴呆等年龄相关病理状态，将寿命延长50%。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
