美國杜克大學(xué)研究人員在新一期《細(xì)胞－代謝》雜志上報(bào)告說,，他們最新完成的動(dòng)物實(shí)驗(yàn)發(fā)現(xiàn),，同時(shí)攝入過多支鏈氨基酸和高脂食品容易導(dǎo)致胰島素抵抗，從而引發(fā)糖尿病等多種疾病,。
研究人員在對實(shí)驗(yàn)鼠進(jìn)行的研究中發(fā)現(xiàn),，同時(shí)攝入過量高脂飼料和支鏈氨基酸的實(shí)驗(yàn)鼠出現(xiàn)胰島素抵抗?fàn)顩r的幾率明顯高于那些攝入普通飼料及適量高脂飼料的實(shí)驗(yàn)鼠。
研究人員分析認(rèn)為,，這是因?yàn)閷?shí)驗(yàn)鼠體內(nèi)一種特定蛋白質(zhì)被激活,，進(jìn)而引發(fā)了胰島素抵抗。他們向?qū)嶒?yàn)鼠喂食能抑制這種蛋白質(zhì)發(fā)揮作用的藥物后,，其胰島素抵抗癥狀消失,。
胰島素抵抗是指機(jī)體對胰島素的敏感性降低,，利用胰島素促進(jìn)葡萄糖代謝的能力下降。胰島素抵抗是Ⅱ型糖尿病,、動(dòng)脈硬化等多種疾病的致病因素,。
研究負(fù)責(zé)人克里斯托弗·紐加德表示，胖人一般都喜歡吃高脂食品,，如果他們還同時(shí)食用較多支鏈氨基酸,，出現(xiàn)胰島素抵抗的風(fēng)險(xiǎn)可能就會(huì)增加，不過這一結(jié)論還需要進(jìn)一步研究加以證實(shí),。
支鏈氨基酸是人體必需但又無法合成的氨基酸,，富含動(dòng)物蛋白的食物支鏈氨基酸的含量一般較高。紐加德說,，從食物中獲取支鏈氨基酸并無過錯(cuò),，但要適可而止。（生物谷Bioon.com）
生物谷推薦原始出處：
Cell Metabolism, 8 April 2009 doi:10.1016/j.cmet.2009.02.002
A Branched-Chain Amino Acid-Related Metabolic Signature that Differentiates Obese and Lean Humans and Contributes to Insulin Resistance
Christopher B. Newgard1,2,3,,,Jie An1,3,James R. Bain1,Michael J. Muehlbauer1,Robert D. Stevens1,Lillian F. Lien1,2,Andrea M. Haqq1,4,Svati H. Shah2,Michelle Arlotto1,Cris A. Slentz2,James Rochon5,Dianne Gallup5,Olga Ilkayeva1,Brett R. Wenner1,William S. Yancy2,Howard Eisenson6,Gerald Musante2,Richard S. Surwit7,David S. Millington1,4,Mark D. Butler1andLaura P. Svetkey1,2
1 Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27710, USA
2 Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
3 Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
4 Department of Pediatrics, Duke University Medical Center, Durham, NC 27710, USA
5 Department of Biostatistics and Informatics, Duke University Medical Center, Durham, NC 27710, USA
6 Department of Community and Family Medicine, Duke University Medical Center, Durham, NC 27710, USA
7 Department of Psychiatry, Duke University Medical Center, Durham, NC 27710, USA
Metabolomic profiling of obese versus lean humans reveals a branched-chain amino acid (BCAA)-related metabolite signature that is suggestive of increased catabolism of BCAA and correlated with insulin resistance. To test its impact on metabolic homeostasis, we fed rats on high-fat (HF), HF with supplemented BCAA (HF/BCAA), or standard chow (SC) diets. Despite having reduced food intake and a low rate of weight gain equivalent to the SC group, HF/BCAA rats were as insulin resistant as HF rats. Pair-feeding of HF diet to match the HF/BCAA animals or BCAA addition to SC diet did not cause insulin resistance. Insulin resistance induced by HF/BCAA feeding was accompanied by chronic phosphorylation of mTOR, JNK, and IRS1Ser307 and by accumulation of multiple acylcarnitines in muscle, and it was reversed by the mTOR inhibitor, rapamycin. Our findings show that in the context of a dietary pattern that includes high fat consumption, BCAA contributes to development of obesity-associated insulin resistance.
