Macro partitioning
High-fat diet (HFD) feeding in mice leads to elevated LSD1 expression and reduced expression of energy-expenditure genes in white adipose tissue, which can be reversed by inhibiting LSD1.
In mice, a high-fat diet increases the levels of LSD1 in fat tissue, which in turn suppresses genes responsible for burning fat. This creates a biological state where the body is less efficient at energy expenditure. Inhibiting LSD1 can reverse this effect, suggesting that targeting this pathway might help counteract the metabolic adaptations caused by high-fat diets.
In the adipose tissues from mice on a high-fat diet, expression of LsD1-target genes is reduced, compared with that in tissues from mice on a normal diet, which can be reverted by suppressing LsD1 function.
Why this rating
In vivo mouse data confirms the in vitro findings in a physiological context of obesity.
Source
FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure
Shinjiro Hino et al. · Nature Communications · 2012
DOI 10.1038/ncomms1755
More from this paper
- Inhibition of the epigenetic regulator LSD1 in adipocytes activates energy-expenditure genes (such as PGC-1α and PDK4), thereby increasing mitochondrial respiration and lipolysis.Good
- LSD1's ability to repress energy-expenditure genes is strictly dependent on cellular FAD (flavin adenine dinucleotide) levels, linking nutritional status to epigenetic control.Good
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