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Daidzein regulates proinflammatory adipokines thereby improving obesity‐related inflammation through PPARγ
Author(s) -
Sakamoto Yuri,
Naka Ayano,
Ohara Nozomi,
Kondo Kazuo,
Iida Kaoruko
Publication year - 2014
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.201300482
Subject(s) - adipokine , daidzein , endocrinology , medicine , adiponectin , proinflammatory cytokine , adipose tissue , chemerin , insulin resistance , adipocyte , inflammation , leptin , chemistry , genistein , insulin , obesity
Scope Daidzein was recently reported to act like an activator of peroxisome proliferator‐activated receptor γ (PPARγ) thereby enhancing differentiation of adipocytes. Although PPARγ plays a role in adipokine expression, it has not been well researched whether daidzein affects expression of adipokines. This study aimed to clarify the effects of daidzein on proinflammatory adipokines and adipose inflammation causing insulin resistance in obesity. Methods and results 3T3‐L1 adipocytes were treated with daidzein or genistein. Diet‐induced obese C57BL/6J mice were fed high‐fat high‐sucrose diets with daidzein (1.0 g/kg chow) for 12 wk. The results showed that both isoflavones, especially daidzein, stimulated adipogenic differentiation in 3T3‐L1 adipocytes with the activation of PPARγ. Daidzein also increased adiponectin expression and decreased MCP‐1 expression with the consistent regulation of their secretion. In obese mice, daidzein inhibited hypertrophy in fat cell size and improved insulin sensitivity, concomitant with upregulation of PPARγ in fat tissue. Decreased expression of MCP‐1 and TNF‐α, and increased expression of adiponectin were also observed in adipose tissue of daidzein‐fed mice. Additionally, daidzein administration significantly inhibited macrophage accumulation in adipose tissue. Conclusion Daidzein regulates adipokine expression through the PPARγ, thereby improving the adverse effects of adipose inflammation, such as insulin resistance, in obesity.