Micronutrients & recovery
LSD1's ability to repress energy-expenditure genes is strictly dependent on cellular FAD (flavin adenine dinucleotide) levels, linking nutritional status to epigenetic control.
The enzyme LSD1, which suppresses fat-burning genes, requires FAD to work. If cellular FAD levels are low, LSD1 cannot repress these genes, leading to increased energy expenditure. This suggests that maintaining adequate levels of riboflavin (Vitamin B2), a precursor to FAD, may support healthy epigenetic regulation of metabolism.
Our data suggest a novel mechanism where LSD1 regulates cellular energy balance through coupling with cellular FAD biosynthesis.
Why this rating
Strong mechanistic evidence showing that impairing FAD synthesis mimics LSD1 inhibition.
Source
FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure
Shinjiro Hino et al. · Nature Communications · 2012
DOI 10.1038/ncomms1755
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- 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
- 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.Good
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