Abstract
Scope: Sonchus Oleraceus, named bitter vegetable (BV), has been known to have multiple health benefits such as anti-aging and anti-inflammation. However, the role of BV in the prevention of obesity is unclear. The aim of this study was to examine the effect of BV lipid extracts (BVL) on obesity development.Methods and Results: Following treatments of high fat diet-induced obese mice (C57BL/6J) with BVL (0.3 mg/g of BW per mouse) for a month, mice exhibited a significant reduction in weight gain, blood triglyceride, and fasting blood glucose compared to control mice. Intriguingly, phosphorylated AMPK, a key regulator of nutrient metabolism, was markedly increased in inguinal fat of BVL group. In 3T3-L1 cells, BVL-7 (100 μg/ml), an omega-3 fatty acid-rich fraction from BVL, lowered lipid accumulation, and down-regulated the gene expression of adipocyte markers. The inhibitory effect of BVL occurred at the early stage of adipocyte differentiation, leading to the delay of mitotic clonal expansion. AMPK knockdown by siRNA abolished the inhibitory effect of BVL-7 on adipogenesis, suggesting that AMPK is essential for BVL-regulated adipocyte differentiation.Conclusion: BVL can effectively inhibit adipogenesis through, at least in part, stimulating AMPK pathway and attenuate HFD-induced obesity. Our findings suggest that BVL can be a promising dietary supplement for protection against obesity, and the effective component of BVL can be potentially developed as anti-obesity drugs.
Highlights
Obesity is mainly developed from energy imbalance, leading to abnormal adipose tissue expansion and subsequently, triggering chronic low-grade inflammation in whole body [1]
The masses of inguinal (Ing) fat and epididymal (Epi) fat in BV lipid extracts (BVL) group were significantly less than C group while muscle mass in BVL group was higher than C group (p < 0.05, Supplementary Table 1)
We found that the fasting blood glucose, plasma insulin level, and plasma TG level were reduced in BVL group relative to control group (Figures 1D–F)
Summary
Obesity is mainly developed from energy imbalance, leading to abnormal adipose tissue expansion and subsequently, triggering chronic low-grade inflammation in whole body [1]. Adipogenesis involves a comprehensive network to form lipid droplets including a cascade of signaling pathway and the stimulation of serial transcriptional factors. Both high-fat diet (HFD)-induced obesity mouse model and murine 3T3-L1 cells as an in vitro model have been used widely for studying adipogenesis. During the early phase of differentiation, growth-arrested 3T3-L1 preadipocytes reenter the cell cycle, which is characterized by mitotic clonal expansion (MCE) followed by the activation of peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT enhancer-binding protein α (C/EBPα) [3], subsequently leading to fatty acids synthesis and adipokine production (e.g., leptin and adiponectin). Activated AMPK has been known to reverse insulin resistance, hyperglyceridemia, and body weight gain [8], which are considered as a therapeutic target of obesity
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