Abstract
There has been a remarkable interest in finding lipid inhibitors from natural products to replace synthetic compounds, and a variety of oriental medicinal herbs are reported to have biological activity with regard to lipid inhibition. Buginawa (Bugi) is a novel combined formula that contains twelve medicinal herbs with potential for weight loss induction. We hypothesized that Bugi may have antiobesity effects in 3T3-L1 preadipocytes and in a high-fat diet- (HFD-) induced mouse model. In this study, 3T3-L1 cells were treated with varied concentrations of Bugi (62.5, 125, or 250 μg/mL). Bugi treatment inhibited adipocyte differentiation by suppressing adipogenic transcription genes, including peroxisome proliferator-activated receptor γ protein (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα), sterol regulatory element-binding protein 1 (SREBP1), and CCAAT/enhancer-binding protein β (C/EBPβ). Mice were fed a normal diet or an HFD for 11 weeks, and Bugi was simultaneously administered at 50 or 100 mg/kg. Bugi administration significantly reduced body weight gain and white adipose tissue (WAT) weight and effectively inhibited lipid droplet accumulation in epididymal white adipose tissue (eWAT) and liver tissue. Further, Bugi treatment suppressed mRNA levels of PPARγ, C/EBPα, and SREBP1 in eWAT and liver tissue. Our findings demonstrate that Bugi could be an effective candidate for preventing obesity and related metabolic disorders.
Highlights
Obesity is known to be a major risk factor for a wide range of noncommunicable diseases including chronic obstructive sleep apnea, type 2 diabetes mellitus (T2DM), and various types of cancers [1]
Differentiation is enhanced by the transcription factor sterol regulatory binding protein 1 (SREBP1), which is promoted by Peroxisome proliferator-activated receptor γ CCAAT/enhancer-binding protein α (C/EBPα) (PPARγ) and controls lipogenic factors involved in fatty acid synthesis [10]
PPARγ, C/EBPα, SREBP, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) oligonucleotide primers were purchased from Bioneer Corporation (Daejeon, Republic of Korea), and SYBR Premix Ex Taq was purchased from Takara Bio Inc. (Otsu, Japan)
Summary
Obesity is known to be a major risk factor for a wide range of noncommunicable diseases including chronic obstructive sleep apnea, type 2 diabetes mellitus (T2DM), and various types of cancers [1]. The cells display an exponential growth phase until confluence is reached, undergo “mitotic clonal expansion (MCE)” that enables an increase in the final proportion of differentiated fat cells, and enter the terminal maturation process of acquiring all the specialized equipment of adipocytes [7]. At the early stage of adipogenesis, transcription factors, including CCAAT/enhancer-binding protein β (C/EBPβ), are induced, thereby stimulating the expression of peroxisome proliferator-activated receptor γ protein (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα) [8]. PPARγ and C/EBPα are regarded as the two main adipogenic transcription factors in this network, positively regulating each other’s expression and acting together to control adipogenesis [9]. It is very important to modulate the gene expression of PPARγ, C/EBPα, and SREBP1 in the study of obesity, since
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