Abstract
Acacetin, a flavone that can be isolated from the Saussurea involucrata plant, has anti-tumor and anti-inflammatory properties that ameliorate airway hyperresponsiveness in asthmatic mice. This study investigated whether acacetin has anti-adipogenic effects in 3T3-L1 adipocytes and whether it regulates the inflammatory response in adipocytes and macrophages. It also investigated whether acacetin ameliorates lipid accumulation in high-fat diet- (HFD) induced obese mice. Differentiated 3T3-L1 cells were treated with acacetin. The glycerol levels in the culture medium were measured, and the expression of proteins and genes involved in adipogenesis and lipolysis were assayed by Western blot and real-time PCR, respectively. Inflammatory cytokine signaling pathway activity was assessed in macrophages that were treated with acacetin and cultured with differentiated medium from 3T3-L1 cells. Intraperitoneal injections of acacetin were administered to HFD-induced obese mice twice a week for 10 weeks. Acacetin significantly increased the levels of glycerol in the culture medium and significantly inhibited lipid accumulation in adipocytes. Acacetin reduced the expression of adipogenesis-related transcription factors, including the expression of the CCAAT/enhancer-binding protein; it also increased sirtuin 1 expression and AMPK phosphorylation in adipocytes. In macrophages cultured with differentiated media from 3T3-L1 adipocytes, acacetin reduced the levels of inflammatory mediators and the activity of the mitogen-activated protein kinase and NF-κB pathways. In obese mice, acacetin reduced both body weight and visceral adipose tissue weight. These results demonstrate that acacetin inhibited adipogenesis in adipocytes and in obese mice. Acacetin also reduced the inflammatory response of macrophages that were stimulated with differentiated media from 3T3-L1 cells.
Highlights
Obesity is a global public health problem that is associated with an increasing prevalence of chronic diseases such as metabolic syndrome, type 2 diabetes, cardiovascular disease, and cancer (Smith and Minson, 2012)
The sterol regulatory element-binding protein 1c (SREBP1c), the CCAAT/enhancer-binding protein (C/EBP), and the peroxisome proliferator-activated receptor (PPAR) protein are all important transcription factors that bind to the promoters of lipogenesis genes, which are involved in the synthesis of fatty acids and triglycerides (Romeo et al, 2012)
Acacetin reduced both the body weight and visceral adipose tissue weight of high-fat diet- (HFD)-induced obese mice and suppressed the expression of genes involved in lipogenesis in murine visceral adipose tissue
Summary
Obesity is a global public health problem that is associated with an increasing prevalence of chronic diseases such as metabolic syndrome, type 2 diabetes, cardiovascular disease, and cancer (Smith and Minson, 2012). Excessive triglyceride levels cause lipids to accumulate, they interfere with the physiological function of adipocytes (Sun et al, 2011). Excessive lipid deposits in adipocytes impair insulin sensitivity and lead to metabolic syndrome abnormalities. The sterol regulatory element-binding protein 1c (SREBP1c), the CCAAT/enhancer-binding protein (C/EBP), and the peroxisome proliferator-activated receptor (PPAR) protein are all important transcription factors that bind to the promoters of lipogenesis genes, which are involved in the synthesis of fatty acids and triglycerides (Romeo et al, 2012). Lipolysis enzymes break down triglycerides to reduce lipid accumulation in adipocytes. Blocking the expression of transcription factors that are important for lipid synthesis will reduce lipid accumulation in adipocytes and reducing the effects of obesity
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