美國研究人員日前報告說,，他們發(fā)現(xiàn)小鼠體重與一種名為FIH的蛋白質(zhì)有關(guān)，這一發(fā)現(xiàn)為研制減肥藥物提供了新思路。
美國加州大學(xué)圣迭戈分校的研究人員在新一期美國《細(xì)胞—代謝》（Cell Metabolism）雜志上報告說，F(xiàn)IH是一種負(fù)責(zé)調(diào)節(jié)缺氧反應(yīng)的蛋白質(zhì),，缺乏這種蛋白質(zhì)的小鼠會保持苗條和健康，哪怕它們進(jìn)食的是高脂肪食物,。
在實驗過程中,，研究人員通過基因技術(shù)培育出缺乏FIH蛋白質(zhì)的實驗鼠，然后讓它們和普通實驗鼠同時進(jìn)食脂肪含量高達(dá)60%的食物,。結(jié)果發(fā)現(xiàn),，缺乏FIH蛋白質(zhì)的實驗鼠平均身材明顯比普通實驗鼠“嬌小”，并且具有更強的新陳代謝能力,。而普通實驗鼠不僅體重增加,，還出現(xiàn)了脂肪肝等。
研究人員表示,，將進(jìn)一步研究FIH蛋白質(zhì)的功能,，以促進(jìn)減肥新藥的研發(fā)。(生物谷Bioon.com)
關(guān)于肥胖的更多閱讀
Nature：解析肥胖基因的蛋白結(jié)構(gòu)
Science：肥胖也是可以傳染的,？
PLoS ONE：發(fā)現(xiàn)可控制肥胖的新基因
生物谷推薦原文出處：
Cell Metabolism doi:10.1016/j.cmet.2010.03.001
The Asparaginyl Hydroxylase Factor Inhibiting HIF-1α Is an Essential Regulator of Metabolism
Na Zhang1, Zhenxing Fu2, Sarah Linke4, Johana Chicher5, Jeffrey J. Gorman5, DeeAnn Visk3, Gabriel G. Haddad3, Lorenz Poellinger6, Daniel J. Peet4, Frank Powell2 and Randall S. Johnson1,
1 Molecular Biology Section, Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA
2 Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA
3 Department of Pediatrics, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA
4 School of Molecular and Biomedical Science, University of Adelaide, Adelaide, SA 5005, Australia
5 Protein Discovery Centre, Queensland Institute of Medical Research, PO Royal Brisbane Hospital, QLD 4029, Australia
6 Karolinska Institute, Stockholm S-17177, Sweden
Factor inhibiting HIF-1α (FIH) is an asparaginyl hydroxylase. Hydroxylation of HIF-α proteins by FIH blocks association of HIFs with the transcriptional coactivators CBP/p300, thus inhibiting transcriptional activation. We have created mice with a null mutation in the FIH gene and found that it has little or no discernable role in mice in altering classical aspects of HIF function, e.g., angiogenesis, erythropoiesis, or development. Rather, it is an essential regulator of metabolism: mice lacking FIH exhibit reduced body weight, elevated metabolic rate, hyperventilation, and improved glucose and lipid homeostasis and are resistant to high-fat-diet-induced weight gain and hepatic steatosis. Neuron-specific loss of FIH phenocopied some of the major metabolic phenotypes of the global null animals: those mice have reduced body weight, increased metabolic rate, and enhanced insulin sensitivity and are also protected against high-fat-diet-induced weight gain. These results demonstrate that FIH acts to a significant degree through the nervous system to regulate metabolism.
