你有没有吃饭后感到无法工作的经历？少吃一点有助于头脑清醒，这可能有科学依据。意大利研究人员在美国新一期《国家科学院学报》上发表报告说，动物实验显示，减少热量摄入可以更持久地保持大脑健康。
罗马圣心天主教大学研究人员发现，与过度进食的实验鼠相比，限制热量摄入的实验鼠不会患糖尿病，认知和记忆能力也更佳。此外，它们不容易患阿尔茨海默氏症（早老性痴呆症），即使患病，时间也会推迟，症状也比过度进食的实验鼠轻。在这项研究中，热量限制意味着实验鼠进食不超过日常所需的70％。
研究人员进一步发现，限制热量摄入激活了实验鼠大脑内的环腺苷酸反应成分结合蛋白1，后者进而能激活其他一系列与长寿相关的分子。而清除该物质后，实验鼠即便限制热量摄入，也会与过度进食者或老年者一样出现大脑功能衰退。
研究人员表示，他们今后的研究方向是通过新药物等方式激活环腺苷酸反应成分结合蛋白1，这样不限制热量摄入也能保持大脑健康。(生物谷 Bioon.com)
doi:10.1073/pnas.1109237109
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A role for neuronal cAMP responsive-element binding (CREB)-1 in brain responses to calorie restriction
Salvatore Fusco, Cristian Ripoli, Maria Vittoria Podda, Sofia Chiatamone Ranieri, Lucia Leone, Gabriele Toietta, Michael W. McBurney, Günther Schütz, Antonella Riccio, Claudio Grassi, Tommaso Galeotti, and Giovambattista Pani
Calorie restriction delays brain senescence and prevents neurodegeneration, but critical regulators of these beneficial responses other than the NAD+-dependent histone deacetylase Sirtuin-1 (Sirt-1) are unknown. We report that effects of calorie restriction on neuronal plasticity, memory and social behavior are abolished in mice lacking cAMP responsive-element binding (CREB)-1 in the forebrain. Moreover, CREB deficiency drastically reduces the expression of Sirt-1 and the induction of genes relevant to neuronal metabolism and survival in the cortex and hippocampus of dietary-restricted animals. Biochemical studies reveal a complex interplay between CREB and Sirt-1: CREB directly regulates the transcription of the sirtuin in neuronal cells by binding to Sirt-1 chromatin; Sirt-1, in turn, is recruited by CREB to DNA and promotes CREB-dependent expression of target gene peroxisome proliferator-activated receptor-γ coactivator-1α and neuronal NO Synthase. Accordingly, expression of these CREB targets is markedly reduced in the brain of Sirt KO mice that are, like CREB-deficient mice, poorly responsive to calorie restriction. Thus, the above circuitry, modulated by nutrient availability, links energy metabolism with neurotrophin signaling, participates in brain adaptation to nutrient restriction, and is potentially relevant to accelerated brain aging by overnutrition and diabetes.
