Abstract
Ferulic acid (FA) is phenolic compound found in fruits. Many studies have reported that FA has diverse therapeutic effects against metabolic diseases. However, the mechanism by which FA modulates adipogenesis via the expression of heme oxygenase-1 (HO-1) implicated in suppression of adipocyte differentiation is not fully understood. We investigated whether HO-1 can be activated by FA and suppress adipogenic factors in 3T3-L1. Our results showed that FA suppresses triglyceride-synthesizing enzymes, fatty acid synthase (FASN) and acetyl-CoA carboxylase (ACC). We observed that the expression of CCAAT/enhancer binding protein α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ) were suppressed by FA. In addition, HO-1 inhibitor stimulated lipid accumulation, while FA attenuated lipid accumulation in 3T3-L1 treated with HO-1 inhibitor. We also observed that the expression of HO-1 had the same tendency as C/EBP homologous protein 10 (CHOP10) during the mitotic clonal expansion (MCE) of adipogenesis. We next employed siRNA against HO-1 to clarify whether HO-1 regulates CHOP10. The results indicated that CHOP10 is downstream of HO-1. Furthermore, FA-mediated HO-1/CHOP10 axis activation prevented the initiation of MCE. Therefore, we demonstrated that FA is a positive regulator of HO-1 in 3T3-L1, and may be an effective bioactive compound to reduce adipocyte tissue mass.
Highlights
Obesity is one of the major risk factors for chronic diseases, including cardiovascular disease, diabetes, and insulin resistance [1]
25, 50, and 100 μM Ferulic acid (FA) were selected for further investigation. 3T3-L1 pre-adipocytes have been used to evaluate the effects of FA on adipogenesis in vitro. 3T3-L1 pre-adipocytes were stimulated with
These results suggested that FA suppresses adipocyte differentiation through the activation of heme oxygenase-1 (HO-1) during the adipogenesis of 3T3-L1 cells
Summary
Obesity is one of the major risk factors for chronic diseases, including cardiovascular disease, diabetes, and insulin resistance [1]. Increasing evidence suggests that obesity causes chronic inflammation via adipocyte-secreted paracrine factors, which prolongs physical pain and affects quality of life [2,3]. Obesity could be treated with medical approaches and diet management, it remains a public health concern. When there is an imbalance between food intake and energy expenditure, adipocytes store energy as intracellular lipids. This process results in enhanced adipogenesis, and obesity [4]. Adipocyte differentiation is stimulated by reactive oxygen species (ROS) in 3T3-L1 cells
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