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Long‐term supplementation of honokiol and magnolol ameliorates body fat accumulation, insulin resistance, and adipose inflammation in high‐fat fed mice
Author(s) -
Kim YoungJe,
Choi MyungSook,
Cha Byung Yoon,
Woo Je Tae,
Park Yong Bok,
Kim Sang Ryong,
Jung Un Ju
Publication year - 2013
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201300113
Subject(s) - endocrinology , medicine , insulin resistance , adiponectin , adipocyte , adipose tissue , resistin , white adipose tissue , chemistry , lipid metabolism , insulin , biology
Scope This study investigated the effect of honokiol ( HON ) and magnolol ( MAG ), phenolic compounds in Magnolia plants, on adiposity and adiposity‐related metabolic disturbances in mice fed high‐fat diet ( HFD ), and the potential underlying mechanisms focusing on the lipid metabolism and inflammatory response. Method and results C 57 BL /6 J mice were fed HFD (45 kcal% fat) with or without HON (0.02%, w/w) or MAG (0.02%, w/w) for 16 wk. Despite no changes in body weight, food intake, and hepatic fat accumulation, HON and MAG significantly lowered the weight of white adipose tissue ( WAT ) as well as adipocyte size and protected against insulin resistance induced by HFD . These effects were associated with increases in energy expenditure and adipose fatty acid oxidation and decreases in fatty acid synthase activity and expression of genes related to fatty acid synthesis, desaturation, and uptake, as well as adipocyte differentiation in WAT . Moreover, HON and MAG significantly lowered the expression of proinflammatory genes in WAT and elevated the plasma IL ‐10 level. Particularly, HON significantly decreased the plasma resistin level and increased the plasma adiponectin level compared to the control group. Conclusion HON and MAG have potential as novel agents for amelioration of adiposity and associated insulin resistance and inflammation.