Flavangenol, one of several pine bark extract products, is expected to prevent
metabolic diseases with its potent
antioxidant effect, its anti-
obesity effect and its improvement of
insulin sensitivity. In this study, targeting the liver as one of the organs that plays an important role in energy metabolism,
Flavangenol was investigated for its effect on
non-alcoholic fatty liver disease (
NAFLD), its action mechanism and its active ingredients, using in vivo and in vitro experiment systems.
Flavangenol suppressed intrahepatic fat accumulation in Western diet-loaded Tsumura Suzuki Obese Diabetes (TSOD) mice, which develop various
metabolic diseases. In addition,
Flavangenol significantly increased the
mRNA expression levels of
fatty acid oxidative
enzymes (peroxisomal proliferator-activated receptor α,
acyl-CoA oxidase,
carnitine palmitoyltransferase). In order to investigate the direct effect of
Flavangenol on the liver, an in vitro
fatty liver model prepared by adding a
free fatty acid to human
liver cancer cells (HepG2 cells) was used. In this model,
Flavangenol significantly suppressed intracellular fat accumulation.
Procyanidin B1, one of the major components of
Flavangenol, also suppressed fat accumulation and induced
mRNA expression of the
fatty acid oxidative
enzymes. As mentioned above,
Flavangenol showed a significant suppressive effect in the
NAFLD model, and it was suggested that the molecular mechanism is induction of
fatty acid oxidation, with the effect mainly attributed to
procyanidin B1.