Abstract
Obesity is prevalent in modern human societies. We examined the anti-obesity effects of scopolin on adipocyte differentiation in preadipocyte 3T3-L1 cells and weight loss in an ovariectomy (OVX)-induced obese mouse model. Scopolin inhibited adipocyte differentiation and lipid accumulation in the preadipocyte cells by suppressing the transcription of adipogenic-related factors, including adiponectin (Adipoq), peroxisome proliferator-activated receptor gamma (Pparg), lipoprotein lipase (Lpl), perilipin1 (Plin1), fatty acid-binding protein 4 (Fabp4), glucose transporter type 4 (Slc2a4), and CCAAT/enhancer-binding protein alpha (Cebpa). In OVX-induced obese mice, administration of scopolin promoted the reduction of body weight, total fat percentage, liver steatosis, and adipose cell size. In addition, the scopolin-treated OVX mice showed decreased serum levels of leptin and insulin. Taken together, these findings suggest that the use of scopolin prevented adipocyte differentiation and weight gain in vitro and in vivo, indicating that scopolin may be a potential bioactive compound for the treatment and prevention of obesity in humans.
Highlights
Obesity is a common metabolic health problem in modern societies [1]
Adipogenic examined whether scopolin inhibited adipocyteindifferentiation differentiation was induced in mouse preadipocyte 3T3-L1 cells with 3-isobutyl-1-methylxanthine, To investigate the anti-obesity effects of the bioactive compound scopolin (Figure 1), we first dexamethasone, and insulin (MDI) in the presence or absence of scopolin (2 and 10 μM)
Adipocyte in the mRNA expression levels of adiponectin (Adipoq), peroxisome proliferator-activated receptor gamma (Pparg), (Lpl), Plin1, fatty acid-binding protein 4 (Fabp4), glucose transporter differentiation was examined by quantitative reverse-transcription PCR and oil red O
Summary
Obesity is associated with an expansion in the size and number of adipocytes, which disrupts energy homeostasis and results in expanded total cholesterol and triacylglycerol (TG) accumulation in the body [2]. Excessive lipid accumulation by adipose tissue is linked to other metabolic disorders, such as type. The differentiation and maturation of adipocytes plays an important role in the induction of obesity-related diseases [6]. Adipocyte differentiation is regulated by several adipogenic transcription factors, including. CCAAT/enhancer-binding proteins (C/EBPs) and peroxisome proliferator-activated receptor gamma which synergistically activate the transcription of downstream target genes such as perilipin 1(Plin 1), fatty acid-binding protein 4, and fatty acid synthase (FAS), leading to fatty acid storage, glucose metabolism, and lipid vacuole formation [7,8]. Lipoprotein lipase in adipocytes is activated by insulin and is involved in the lipolysis of circulating lipoproteins for the subsequent uptake by adipocytes [9]
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