Emodin Protects against High-Fat Diet-Induced Obesity via Regulation of AMP-Activated Protein Kinase Pathways in White Adipose Tissue

Abstract

Emodin is an active herbal component traditionally used in China for treating a variety of diseases. The aim of this study was to examine the effect of emodin on the reducing lipid accumulation in white adipose tissue of high-fat diet-fed rats, and on the regulation of the expression of the genes involved in lipid metabolism to elucidate the mechanisms. After being fed a high-fat diet for two weeks, rats were dosed orally with emodin (20, 40, 80 mg/kg/day) or pioglitazone (20 mg/kg/day), once daily for eight weeks. Changes in body weight, feeding pattern, serum lipids, coronary artery risk index, and atherogenic index were investigated. Subcutaneous white adipose tissues were isolated for pathology histology and Western blot analyses. Changes of triglyceride accumulation in differentiated 3 T3-L1 adipocytes were also investigated. Emodin exhibited a significant concentration-dependent decrease in the intracellular accumulation of triglyceride in 3 T3-L1 adipocytes. Emodin (80 mg/kg/day) displayed similar characteristics to pioglitazone (20 mg/kg/day) in reducing body weight gain and plasma lipid levels as well as the coronary artery risk and atherogenic indices of high-fat diet-fed rats. Emodin also caused dose related reductions in epididymal white adipose tissue sizes in high-fat diet-fed rats. Emodin and pioglitazone enhanced the phosphorylation of AMP-activated protein kinase and its primary downstream targeting enzyme, acetyl-CoA carboxylase, upregulated gene expression of carnitine palmitoyl transferase 1, and downregulated sterol regulatory element binding protein 1 and fatty acid synthase protein levels in the epididymal white adipose tissue of high-fat diet-fed rats. Our findings suggest that emodin could attenuate lipid accumulation in white adipose tissue through AMP-activated protein kinase activation.

Emodin Regulates Glucose Utilization by Activating AMP-activated Protein Kinase*

“…8, A and B). In fact, a very recent paper also reports that emodin increases AMPK and ACC in hepatocytes and adipose tissues of high fat diet-fed rats and improves dyslipidemia after 8 weeks of treatment (41,42).…”

Anti-leukemic activity of a four-plant mixture in a leukemic rat model

“…acetosella and R. palmatum contain emodin and chrysophanic acid (Tamayo et al, 2000) which are anthraquinone derivatives reported to have cytotoxic, antitumorigenic, antioxidant properties, and immunosuppressive properties (Yim et al, 1999;Zhang, Lau, Xia, Hortobagyi, & Hung, 1999;Süleyman, Demirezer, Kuruüzüm-Uz, & Akçay, 2002;Tzeng, Lu, Liou, Chang, & Liu, 2012). In addition, Rumex plants contain other anthraquinones like physcion, aloe emodin, rhein, barbaloin, sennoside A, and sennoside B (Wegiera, Smolarz, Wianowska, & Dawidowicz, 2007), and they all showed various pharmacological properties, such as antitumor (Kimura, Sumiyoshi, Taniguchi, & Baba, 2008), antimutagenic (Lee et al, 2005), and antioxidant activities (Demirezer, Kuruüzüm-Uz, Bergere, Schiewe, & Zeeck, 2001).…”

Synergistic interactions of apigenin, naringin, quercetin and emodin on inhibition of 3T3-L1 preadipocyte differentiation and pancreas lipase activity

“…Moreover, active compounds naturally co-exist in the diet. In this study, we chose four compounds including apigenin, naringin, quercetin and emodin, all of which were reported to possess the ability of inhibiting adipogenesis [8,11,12,23], to investigate the effect of the four compounds in binary combinations on preventing obesity, which was rarely reported in previous reports.…”

“…In addition, apigenin could activate 5 -adenosine monophosphate-activated protein kinase (AMPK) in a dose-dependent manner, which is known to suppress adipogenesis [8]. Previous reports claimed that emodin enhanced the phosphorylation of AMPK and its primary downstream targeting enzyme, acetyl-CoA carboxylase, and downregulated sterol regulatory element-binding proteins (SREBP1) and fatty acid synthase protein levels in the epididymal white adipose tissue of high-fat diet-fed rats [12]. Compounds such as apigenin and emodin with different modes of action might exhibit synergism resulted from a sequential blockade, concurrent inhibition, or complementary inhibition [24].…”

“…Quercetin, a kind of flavonol, inhibited cell growth, differentiation and induced apoptosis in 3T3-L1 preadipocytes [11] and was reported as a strong inhibitor of pancreatic lipase [4]. Emodin has also been demonstrated as an active herbal component with the ability to inhibit cell proliferation and differentiation of 3T3-L1 preadipocytes [12] and could act as a pancreatic lipase inhibitor [13].…”