美国杜克大学研究人员在新一期《细胞－代谢》杂志上报告说，他们最新完成的动物实验发现，同时摄入过多支链氨基酸和高脂食品容易导致胰岛素抵抗，从而引发糖尿病等多种疾病。
研究人员在对实验鼠进行的研究中发现，同时摄入过量高脂饲料和支链氨基酸的实验鼠出现胰岛素抵抗状况的几率明显高于那些摄入普通饲料及适量高脂饲料的实验鼠。
研究人员分析认为，这是因为实验鼠体内一种特定蛋白质被激活，进而引发了胰岛素抵抗。他们向实验鼠喂食能抑制这种蛋白质发挥作用的药物后，其胰岛素抵抗症状消失。
胰岛素抵抗是指机体对胰岛素的敏感性降低，利用胰岛素促进葡萄糖代谢的能力下降。胰岛素抵抗是Ⅱ型糖尿病、动脉硬化等多种疾病的致病因素。
研究负责人克里斯托弗·纽加德表示，胖人一般都喜欢吃高脂食品，如果他们还同时食用较多支链氨基酸，出现胰岛素抵抗的风险可能就会增加，不过这一结论还需要进一步研究加以证实。
支链氨基酸是人体必需但又无法合成的氨基酸，富含动物蛋白的食物支链氨基酸的含量一般较高。纽加德说，从食物中获取支链氨基酸并无过错，但要适可而止。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
