TY - JOUR
T1 - Regulation of branched-chain amino acid catabolism in rat models for spontaneous type 2 diabetes mellitus
AU - Kuzuya, Teiji
AU - Katano, Yoshiaki
AU - Nakano, Isao
AU - Hirooka, Yoshiki
AU - Itoh, Akihiro
AU - Ishigami, Masatoshi
AU - Hayashi, Kazuhiko
AU - Honda, Takashi
AU - Goto, Hidemi
AU - Fujita, Yuko
AU - Shikano, Rie
AU - Muramatsu, Yuji
AU - Bajotto, Gustavo
AU - Tamura, Tomohiro
AU - Tamura, Noriko
AU - Shimomura, Yoshiharu
N1 - Funding Information:
This work was supported in part by a Grant-in-Aid for Scientific Research (17300208 and 20300216 to Y.S.) from the Ministry of Education, Culture, Sports, Science and Technology of Japan and a grant from the Uehara Memorial Foundation (to Y.S.).
PY - 2008/8/15
Y1 - 2008/8/15
N2 - The branched-chain α-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.
AB - The branched-chain α-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.
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U2 - 10.1016/j.bbrc.2008.05.167
DO - 10.1016/j.bbrc.2008.05.167
M3 - Article
C2 - 18541149
AN - SCOPUS:45849128681
SN - 0006-291X
VL - 373
SP - 94
EP - 98
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -
