瑞典卡羅林斯卡醫(yī)學(xué)院15日宣布,，該機(jī)構(gòu)專家發(fā)現(xiàn)心臟血管和肌肉能自發(fā)調(diào)節(jié)日常攝入食物中的脂肪酸，這對(duì)治療包括Ⅱ型糖尿病在內(nèi)的新陳代謝疾病有重要意義,。
卡羅林斯卡醫(yī)學(xué)院的研究人員用老鼠進(jìn)行了實(shí)驗(yàn)，他們將VEGF－B蛋白質(zhì)作為從肌肉到血管壁的傳導(dǎo)信號(hào),，對(duì)其生物功能進(jìn)行測試后發(fā)現(xiàn),，該蛋白質(zhì)能控制血管壁中的脂肪酸運(yùn)輸?shù)鞍踪|(zhì)（FATPs）的數(shù)量。
瑞典專家指出,，當(dāng)FATPs蛋白質(zhì)增多時(shí),，從血管壁穿過并被攝入的脂肪也相應(yīng)迅速增加。那些血管壁中缺乏VEGF－B蛋白質(zhì)受體的老鼠,，其肌肉和心臟中攝入的脂肪較少,，在不同機(jī)體組織中積聚的脂肪也比較少。
研究項(xiàng)目負(fù)責(zé)人,、卡羅林斯卡醫(yī)學(xué)院的醫(yī)藥生物化學(xué)和生物物理學(xué)教授烏爾夫·埃里克松說,，由于肌肉中的脂肪過度增加是造成人體出現(xiàn)胰島素抵抗進(jìn)而罹患Ⅱ型糖尿病的重要原因，因此上述發(fā)現(xiàn)對(duì)于治療包括Ⅱ型糖尿病在內(nèi)的新陳代謝疾病有重要意義,。這一研究成果已發(fā)表在最新一期英國《自然》Nature雜志上,。
據(jù)埃里克松等人介紹，下一步他們將致力于研究如何影響胰島素信號(hào),，并且通過調(diào)節(jié)VEGF－B蛋白質(zhì)信號(hào)來降低患糖尿病老鼠的血液葡萄糖水平,。（生物谷Bioon.com）
生物谷推薦原文出處：
Nature doi:10.1038/nature08945
Vascular endothelial growth factor B controls endothelial fatty acid uptake
Carolina E. Hagberg1,2, Annelie Falkevall1,2, Xun Wang1,2, Erik Larsson3, Jenni Huusko4, Ingrid Nilsson1, Laurens A. van Meeteren5, Erik Samen6,7, Li Lu7, Maarten Vanwildemeersch1,2, Joakim Klar2,5, Guillem Genove8, Kristian Pietras1,2, Sharon Stone-Elander6,7, Lena Claesson-Welsh5, Seppo Yl?-Herttuala4, Per Lindahl3,9 & Ulf Eriksson1,2
Tissue Biology Group, Division of Matrix Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-171 77 Stockholm, SwedenLudwig Institute for Cancer Research Ltd, Stockholm Branch, Karolinska Institutet, Box 240, SE-171 77 Stockholm, Sweden
Institute of Biomedicine, University of Gothenburg, Box 440, SE-405 30 Gothenburg, Sweden
Department of Biotechnology and Molecular Medicine, A.I. Virtanen Institute, University of Kuopio, Box 1627, FIN-70211 Kuopio, Finland
Uppsala University, Department of Genetics and Pathology, Rudbeck Laboratory, SE-751 85 Uppsala, Sweden
Karolinska Pharmacy, Karolinska University Hospital, Solna, SE-17176 Stockholm, Sweden
Clinical Neurosciences, Karolinska Institutet, SE-171 76 Stockholm, Sweden
Laboratory of Vascular Biology, Division of Matrix Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, SE-171 77 Stockholm, Sweden
Wallenberg Laboratory for Cardiovascular Research, Bruna Str?ket 16, Sahlgrenska University Hospital, SE-413 45 Gothenburg, Sweden
The vascular endothelial growth factors (VEGFs) are major angiogenic regulators and are involved in several aspects of endothelial cell physiology1. However, the detailed role of VEGF-B in blood vessel function has remained unclear2, 3. Here we show that VEGF-B has an unexpected role in endothelial targeting of lipids to peripheral tissues. Dietary lipids present in circulation have to be transported through the vascular endothelium to be metabolized by tissue cells, a mechanism that is poorly understood4. Bioinformatic analysis showed that Vegfb was tightly co-expressed with nuclear-encoded mitochondrial genes across a large variety of physiological conditions in mice, pointing to a role for VEGF-B in metabolism. VEGF-B specifically controlled endothelial uptake of fatty acids via transcriptional regulation of vascular fatty acid transport proteins. As a consequence, Vegfb-/- mice showed less uptake and accumulation of lipids in muscle, heart and brown adipose tissue, and instead shunted lipids to white adipose tissue. This regulation was mediated by VEGF receptor 1 and neuropilin 1 expressed by the endothelium. The co-expression of VEGF-B and mitochondrial proteins introduces a novel regulatory mechanism, whereby endothelial lipid uptake and mitochondrial lipid use are tightly coordinated. The involvement of VEGF-B in lipid uptake may open up the possibility for novel strategies to modulate pathological lipid accumulation in diabetes, obesity and cardiovascular diseases.
