
This study hypothesized that BCAAs could alter the hepatic oxidative function and de novo lipogenesis, independent of them being anaplerotic substrates for the mitochondria. A greater induction of lipid oxidation and ketogenesis upon fasting was evident in LB mice's BCAA-supplemented, insulin-sensitive livers. At the same time, their hepatic de novo lipogenesis rates remained lower than their LF counterparts. Taken together, our results provide evidence that BCAA supplementation, under conditions of insulin sensitivity, improved the feeding-to-fasting induction of hepatic lipid oxidation through changes in cellular redox, thus providing a favourable biochemical environment for flux through β-oxidation and lower de novo lipogenesis.
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