你有沒有吃飯后感到無法工作的經(jīng)歷,？少吃一點有助于頭腦清醒,，這可能有科學依據(jù)。意大利研究人員在美國新一期《國家科學院學報》上發(fā)表報告說,，動物實驗顯示,，減少熱量攝入可以更持久地保持大腦健康。
羅馬圣心天主教大學研究人員發(fā)現(xiàn),，與過度進食的實驗鼠相比,，限制熱量攝入的實驗鼠不會患糖尿病，認知和記憶能力也更佳,。此外,，它們不容易患阿爾茨海默氏癥（早老性癡呆癥），即使患病,，時間也會推遲,，癥狀也比過度進食的實驗鼠輕。在這項研究中,，熱量限制意味著實驗鼠進食不超過日常所需的70％,。
研究人員進一步發(fā)現(xiàn)，限制熱量攝入激活了實驗鼠大腦內(nèi)的環(huán)腺苷酸反應成分結(jié)合蛋白1,，后者進而能激活其他一系列與長壽相關(guān)的分子,。而清除該物質(zhì)后，實驗鼠即便限制熱量攝入,，也會與過度進食者或老年者一樣出現(xiàn)大腦功能衰退。
研究人員表示,，他們今后的研究方向是通過新藥物等方式激活環(huán)腺苷酸反應成分結(jié)合蛋白1,，這樣不限制熱量攝入也能保持大腦健康。(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.
