Abstract
This study assessed the effects of Coprinus comatus cap (CCC) on adipogenesis in 3T3-L1 adipocytes and the effects of CCC on the development of diet-induced obesity in rats. Here, we showed that the CCC has an inhibitory effect on the adipocyte differentiation of 3T3-L1 cells, resulting in a significant decrease in lipid accumulation through the downregulation of several adipocyte specific-transcription factors, including CCAAT/enhancer binding protein β, C/EBPδ, and peroxisome proliferator-activated receptor gamma (PPARγ). Moreover, treatment with CCC during adipocyte differentiation induced a significant down-regulation of PPARγ and adipogenic target genes, including adipocyte protein 2, lipoprotein lipase, and adiponectin. Interestingly, the CCC treatment of the 3T3-L1 adipocytes suppressed the insulin-stimulated Akt and GSK3β phosphorylation, and these effects were stronger in the presence of an inhibitor of Akt phosphorylation, LY294002, suggesting that CCC inhibited adipocyte differentiation through the down-regulation of Akt signaling. In the animal study, CCC administration significantly reduced the body weight and adipose tissue weight of rats fed a high fat diet (HFD) and attenuated lipid accumulation in the adipose tissues of the HFD-induced obese rats. The size of the adipocyte in the epididymal fat of the CCC fed rats was significantly smaller than in the HFD rats. CCC treatment significantly reduced the total cholesterol and triglyceride levels in the serum of HFD rats. These results strongly indicated that the CCC-mediated decrease in body weight was due to a reduction in adipose tissue mass. The expression level of PPARγ and phospho-Akt was significantly lower in the CCC-treated HFD rats than that in the HFD obesity rats. These results suggested that CCC inhibited adipocyte differentiation by the down-regulation of major transcription factor involved in the adipogenesis pathway including PPARγ through the regulation of the Akt pathway in 3T3-L1 cells and HFD adipose tissue.
Highlights
Obesity is associated with various diseases, cardiovascular disease, type 2 diabetes, and metabolic diseases, including metabolic syndrome [1]
Obesity is induced by increases in adipose tissue mass, which results from the multiplication of fat cells through adipogenesis and increased deposition of cytoplasmic triglycerides [29]
We demonstrated that Coprinus comatus cap extracts (CCCE) significantly inhibited adipogenesis and adipocyte differentiation in 3T3-L1 cells through the regulation of peroxisome proliferator-activated receptor gamma (PPARc) activation and the Akt signaling pathway, leading to decreases in body weight and fat tissue mass in high-fat diet (HFD)-induced obese rats
Summary
Obesity is associated with various diseases, cardiovascular disease, type 2 diabetes, and metabolic diseases, including metabolic syndrome [1]. Cellular and molecular studies concerning obesity have shown that increased numbers of adipocytes, which are associated with alterations in size, are triggered by genetic or dietary factors [3]. The differentiation of preadipocytes into adipocytes is accompanied by a dramatic increase in the expression of CCAAT/ enhancer binding protein b (C/EBPb) and C/EBPd, which transcriptionally activate the C/EBPa and peroxisome proliferator-activated receptor gamma (PPARc) genes by binding to the C/ EBP regulatory elements [5,6]. PPARc is considered the master regulator of adipocyte differentiation and drives the expression of adipocyte-specific genes. The activation of PPARc is necessary for the expression of adipocyte-specific genes, such as adipocyte protein 2 (aP2), lipoprotein lipase (LPL), and adiponectin and fatty acid synthase (FAS), which facilitates the cytoplasmic storage of massive amounts of triglycerides [7]
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