Abstract
Obesity, a chronic metabolic disorder, is characterized by enlarged fat mass and dysregulation of lipid metabolism. The medicinal plant, Boesenbergia pandurata (Roxb.) Schltr., has been reported to possess anti-oxidative and anti-inflammatory properties; however, its anti-obesity activity is unexplored. The present study was conducted to determine whether B. pandurata extract (BPE), prepared from its rhizome parts, attenuated high-fat diet (HFD)-induced obesity in C57BL/6J mice. The molecular mechanism was investigated in 3T3-L1 adipocytes and HepG2 human hepatoma cells. BPE treatment decreased triglyceride accumulation in both 3T3-L1 adipocytes and HepG2 hepatocytes by activating AMP-activated protein kinase (AMPK) signaling and regulating the expression of lipid metabolism-related proteins. In the animal model, oral administration of BPE (200 mg/kg/day for 8 weeks) significantly reduced HFD-induced body weight gain without altering the amount of food intake. In addition, elevated serum levels of total cholesterol, low-density lipoprotein cholesterol, and triglycerides were suppressed by BPE administration. Fat pad masses were reduced in BPE-treated mice, as evidenced by reduced adipocyte size. Furthermore, BPE protected against the development of nonalcoholic fatty liver by decreasing hepatic triglyceride accumulation. BPE also activated AMPK signaling and altered the expression of lipid metabolism-related proteins in white adipose tissue and liver. Taken together, these findings indicate that BPE attenuates HFD-induced obesity by activating AMPK and regulating lipid metabolism, suggesting a potent anti-obesity agent.
Highlights
Obesity is a chronic metabolic disorder caused by an energy imbalance
These results suggest that B. pandurata extract (BPE) reduces TG accumulation in two ways: by downregulating the expression of proteins involved in lipogenesis and by upregulating proteins in the Because AMPK is a key regulator of proteins involved in lipogenesis and fatty acid oxidation (FAO) in metabolic tissues [12], we investigated whether BPE activated AMPK by assessing its level of phosphorylation
Histological analysis of the S.C fat pad indicated that the BPE-induced reduction in fat pad mass was principally due to decreased adipocyte size (Figure 3B). These results indicate that BPE reduces fat mass by attenuating adipocyte enlargement, and this suggests an anti-adipogenic effect of BPE
Summary
Obesity is a chronic metabolic disorder caused by an energy imbalance. A long-term excess of energy intake over energy expenditure results in the storage of excess energy as fat [1,2]. Lipogenic proteins, including acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), stearoyl-CoA desaturase (SCD), and peroxisome proliferator-activated receptor γ (PPARγ), are expressed predominantly in adipocytes and hepatocytes. These proteins are upregulated by sterol regulatory element-binding protein 1c (SREBP-1c), which is a key transcription factor upregulating de novo lipogenesis [8]. FFAs and cholesterol, which results in insulin resistance Proteins, such as PPARα, carnitine palmitoyl transferase 1 (CPT-1), and uncoupling proteins (UCPs), increase FAO and fatty acid clearance. AMPK is known to increase the expression of proteins involved in fatty acid β-oxidation, including PPARα, PPARγ coactivator-1α (PGC-1α), CPT-1, and UCPs [14]. The anti-obesity effects of B. pandurata extract (BPE) and its molecular mechanisms were characterized in vitro and in vivo
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