Energy balance
Inhibition of the epigenetic regulator LSD1 in adipocytes activates energy-expenditure genes (such as PGC-1α and PDK4), thereby increasing mitochondrial respiration and lipolysis.
This research identifies LSD1 as a key epigenetic regulator that suppresses energy expenditure in fat cells. Inhibiting LSD1 (through genetic knockdown or specific inhibitors like tranylcypromine) reverses this suppression, leading to increased mitochondrial activity and fat burning. While direct LSD1 inhibition is not yet a standard human therapy, this mechanism highlights the importance of cellular FAD availability and epigenetic control in metabolic health.
Disruption of LSD1 function resulted in the de-repression of these genes leading to the activation of mitochondrial respiration and lipolysis in adipocytes.
Why this rating
High-quality peer-reviewed research (Nature Communications) with robust in vitro and in vivo mouse data, though not a human clinical trial.
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
- 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
- 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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