Research

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.

GoodSupportsHIGH confidence
Disruption of LSD1 function resulted in the de-repression of these genes leading to the activation of mitochondrial respiration and lipolysis in adipocytes.
Shinjiro Hino et al. · Nature Communications · 2012

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

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DOI resolved against Crossref · corpus check 2026-06-10

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