Regulation of branched-chain amino acid catabolism in rat models for spontaneous type 2 diabetes mellitus

被引:55
作者
Kuzuya, Teiji [2 ]
Katano, Yoshiaki [2 ]
Nakano, Isao [2 ]
Hirooka, Yoshiki [2 ]
Itoh, Akihiro [2 ]
Ishigami, Masatoshi [2 ]
Hayashi, Kazuhiko [2 ]
Honda, Takashi [2 ]
Goto, Hidemi [2 ]
Fujita, Yuko [1 ]
Shikano, Rie [1 ]
Muramatsu, Yuji [1 ]
Bajotto, Gustavo [1 ]
Tamura, Tomohiro [3 ]
Tamura, Noriko [3 ]
Shimomura, Yoshiharu [1 ]
机构
[1] Nagoya Inst Technol, Dept Mat Sci & Engn, Showa Ku, Nagoya, Aichi 4668555, Japan
[2] Nagoya Univ, Grad Sch Med, Dept Gastroenterol, Showa Ku, Nagoya, Aichi 4668550, Japan
[3] Natl Inst Adv Ind Sci & Technol, Res Inst Genome Based Biofactory, Toyohira Ku, Sapporo, Hokkaido 0628517, Japan
关键词
branched-chain amino acid (BCAA); type 2 diabetes mellitus; branched-chain alpha-keto acid dehydrogenase (BCKDH) complex; BCKDH kinase; Otsuka Long-Evans Tokushima Fatty (OLETF) rat;
D O I
10.1016/j.bbrc.2008.05.167
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:94 / 98
页数:5
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