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Dietary L‐lysine supplementation reduces de novo lipogenesis via AMPK activation and malonyl‐CoA suppression
Author(s) -
Hirabayashi Yuri,
Murakami Hitoshi,
Inoue Yoshiko,
Fujieda Takeshi,
Kobayashi Hisamine
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.227.6
Subject(s) - lipogenesis , ampk , lysine , endocrinology , medicine , chemistry , palmitic acid , skeletal muscle , beta oxidation , fatty acid , phosphorylation , metabolism , biochemistry , biology , amino acid , protein kinase a
We reported that dietary L‐lysine supplementation increased fat oxidation in mice fed a high‐fat diet (EB 2006). Dietary L‐lysine supplementation also decreases diet induced obesity as well as hyperlipidemia. In this experiment, we investigated the effect of L‐lysine on de novo lipogenesis, malonyl‐CoA content, and AMPK activation. (Exp1) Male C57BL/6J mice were injected i.p. with 2 H 2 O and fed a normal diet (LF; 5% fat w/w) or the diet supplemented with 3.0 % L‐lysine monohydrochloride (Lys) for an hour. 2 H labeling of palmitic acid and water in plasma were measured, and fractional synthesis rate (FSR) of palmitic acid was calculated. The result showed that Lys suppressed FSR of palmitic acid (LF: 2.78±0.68 %/h vs Lys: 1.91±0.32 %/h). (Exp2) Male C57BL/6J mice were fed a high‐fat diet (HF; 25% fat w/w) or the high‐fat diet supplemented with 3.0% Lys for 8 hours in dark period. Malonyl‐CoA contents and phosphorylation level of AMPK in liver and skeletal muscle were measured. Malonyl‐CoA content of liver in Lys group was less than that in HF group during feeding period. P‐AMPK/AMPK level was increased by L‐lysine at 2 and 4 hours after feeding in liver (2h: 1.27 fold, 4h: 1.36 fold). In skeletal muscle, Lys didn't affect malonyl‐CoA content and P‐AMPK/AMPK level. In conclusion, our data suggests that dietary supplementation of L‐lysine increases fat oxidation and inhibits de novo lipogenesis via AMPK activation and malonyl‐CoA suppression in liver.