The
flavonoid myricitrin exhibits various pharmacological and physiological effects. However, studies on the effects of
myricitrin on
obesity are limited. We hypothesized that dietary
myricitrin would attenuate the adiposity and metabolic dysfunction that occur in
obesity. To test this hypothesis, mice were randomly fed a high-fat diet (HFD) or HFD supplemented with
myricitrin for 16 weeks.
Myricitrin significantly reduced white adipose tissue (WAT) mass, adipocyte size, and plasma
leptin levels, and also attenuated
dyslipidemia. These changes appeared to result from increased energy expenditure and activation of the
carnitine acyltransferase (
CPT) and β-oxidation in WAT. Expressions of the proinflammatory genes NF-κB, TLR2, MCP1, and TNF-α were also lower in the WAT of
myricitrin-supplemented mice. Moreover,
myricitrin markedly reduced hepatic
triglyceride accumulation and plasma
aspartate transaminase levels by increasing
CPT activity and reducing
fatty acid synthase activity in the liver.
Myricitrin-supplemented mice also showed improved
glucose tolerance,
insulin sensitivity, and decreased
hyperinsulinemia, along with decreased levels of circulating
resistin. In conclusion, long-term consumption of a
myricitrin-supplemented diet may effectively protect against HFD-induced
obesity and related metabolic disorders.