Regulation of branched-chain amino acid catabolism in rat models for spontaneous type 2 diabetes mellitus
Regulation of branched-chain amino acid catabolism in rat models for spontaneous type 2 diabetes mellitus
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DOI：
10.1016/j.bbrc.2008.05.167
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发表时间：
2008-08-15
影响因子：
3.1
通讯作者：
Shimomura, Yoshiharu
中科院分区：
文献类型：
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作者：
Kuzuya, Teiji;Katano, Yoshiaki;Shimomura, Yoshiharu
支链α-酮酸脱氢酶（BCKDH）复合物是支链氨基酸（BCAA）催化过程中最重要的调节酶。我们研究了自发性2型糖尿病大冢龙-埃文斯德岛脂肪（OLETF）大鼠和Zucker糖尿病脂肪大鼠肝脏BCKDH复合物活性的调节。肝BCKDH复合物活性明显低于相应对照组。OLETF大鼠BCKDH复合物的量与复合物的总活性相对应。BCKDH激酶的结合形式，这是负责复合物的失活的活性和丰度，表现出反相关性BCKDH复合物的活性在OLETF大鼠。连续10周补充5%BCAAs可显著提高大鼠BCKDH复合物活性，降低BCKDH激酶活性和结合形式。这些结果表明，2型糖尿病患者的BCAA catalysts被BCAA补充剂下调和增强。(C)2008年爱思唯尔公司All rights reserved.
The branched-chain alpha-keto acid dehydrogenase (BCKDH) complex is the most important regulatory enzyme in branched-chain amino acid (BCAA) catabolism. We examined the regulation of hepatic BCKDH complex activity in spontaneous type 2 diabetes Otsuka Long-Evans Tokushima Fatty (OLETF) rats and Zucker diabetic fatty rats. Hepatic BCKDH complex activity in these rats was significantly lower than in corresponding control rats. The amount of BCKDH complex in OLETF rats corresponded to the total activity of the complex. Activity and abundance of the bound form of BCKDH kinase, which is responsible for inactivation of the complex, showed an inverse correlation to BCKDH complex activity in OLETF rats. Dietary supplementation of 5% BCAAs for 10 weeks markedly increased BCKDH complex activity, and decreased the activity and bound form of BCKDH kinase in the rats. These results suggest that BCAA catabolism in type 2 diabetes is downregulated and enhanced by BCAA supplementation. (C) 2008 Elsevier Inc. All rights reserved.