Activity In 3T3-L1 Adipocytes Research Articles

A combination of commercial and traditional food-source-derived enzymatic treatment acts as a potential tool to produce functional yuzu (Citrus junos) powder

Enzymatic modifications have been applied in citrus to enhance their physicochemical and biological properties and reduce their bitterness. Notwithstanding, research on the combination of enzyme treatment of yuzu is lacking. In this study, yuzu was treated with a combination of isolated cellulase NY203, pectinase UF, and cellulase KN, and this enzymatic treatment was found to increase monosaccharide, naringenin, and hesperetin levels. In contrast, dietary fiber, cellulose, hemicellulose, lignin, and pectin levels were decreased. Moreover, the enzymes disintegrated the inner and outer surface structures and chemical bonding of yuzu, thus improving its solubility rate, water-holding capacity, oil-adsorption capacity, cholesterol-binding capacity, and water-swelling capacity. Furthermore, NY203 + UF + KN combination treatment reduced the bitterness of treated yuzu by 50 % compared with the control. Additionally, NY203 + UF + KN treatment yielded a 28 % decrease in lipid accumulation and two-fold higher lipolytic activity in 3T3L-1 adipocytes. These findings are potentially beneficial to the food/nutraceutical industries regarding functional yuzu powder production.

Protopanaxadiol-Enriched Rice Exerted Antiadipogenic Activity during 3T3-L1 Differentiation and Anti-Inflammatory Activity in 3T3-L1 Adipocytes.

Ginseng is a traditional medicine with health benefits for humans. Protopanaxadiol (PPD) is an important bioactive compound found in ginseng. Transgenic rice containing PPD has been generated previously. In the present study, extracts of this transgenic rice were evaluated to assess their antiadipogenic and anti-inflammatory activities. During adipogenesis, cells were treated with transgenic rice seed extracts. The results revealed that the concentrations of the rice seed extracts tested in this study did not affect cell viability at 3 days post-treatment. However, the rice seed extracts significantly reduced the accumulation of lipids in cells and suppressed the activation of CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), which in turn inhibited the expression of adipogenesis-related mRNAs, such as adiponectin, PPARγ, C/EBPα, sterol regulatory element-binding protein 1, glucose transport member 4, and fatty acid synthase. In adipocytes, the extracts significantly reduced the mRNA expression of inflammation-related factors following LPS treatment. The activation of NF-κB p65 and ERK 1/2 was inhibited in extract-treated adipocytes. Moreover, treatment with extract #8 markedly reduced the cell population of the G2/M phase. Collectively, these results indicate that transgenic rice containing PPD may act as an obesity-reducing and/or -preventing agent.

Anti-Obesity Effect of Sodium Selenite through Inhibitory Regulation of Epigenetic Enzyme Activity in 3T3-L1 Adipocytes

Jae-In Lee, Min-Yu Chung, Seon Kyeong Park, Seul-Min Hong, Young-Soo Kim, and Jae-Ho Park. Journal of the Korean Society of Food Science and Nutrition 2023;52:241-9. https://doi.org/10.3746/jkfn.2023.52.3.241

Dopaminergic and adrenergic receptors synergistically stimulate browning in 3T3-L1 white adipocytes.

The browning of white adipose tissue (WAT) has attracted considerable attention in the scientific community as a popular strategy for enhancing energy expenditure to combat obesity. As a part of this strategy, β3-adrenergic receptor (β3-AR) is the most widely studied receptor that mediates thermogenesis. Parenthetically, further studies in search for additional receptors expressed in adipocytes that can mediate thermogenesis has been appearing, and this paper reports that dopaminergic receptor 1 (DRD1) and β3-AR synergistically stimulate browning in 3T3-L1 white adipocytes. qRT-PCR and immunoblot analysis methods were applied to evaluate the effects of DRD1 on the target proteins downstream of β3-AR and other markers involved in lipid metabolism, mitochondrial biogenesis, and browning events. These results show that DRD1 is expressed in epididymal WAT (eWAT), brown adipose tissue (BAT), and inguinal WAT (iWAT) of normal and high-fat-fed mice, and a deficiency of DRD1 downregulates the expression of brown adipocyte-specific proteins. Silencing of DRD1 affected lipid metabolic activity in 3T3-L1 adipocytes by reducing mitochondrial biogenesis as well as levels of lipolytic and fat oxidative marker proteins in a similar pattern to β3-AR. Moreover, mechanistic studies showed that the depletion of DRD1 downregulates β3-AR and its downstream molecules, suggesting both receptors might synergistically stimulate browning. Parallel to the UCP1-dependent thermogenesis, the depletion of DRD1 also downregulates the expression of core proteins responsible for UCP1-independent thermogenesis. Overall, DRD1 mediates β3-AR-dependent 3T3-L1 browning and UCP1-independent thermogenesis.

Pomolic acid in persimmon peel suppresses the increase in glycerol-3 phosphate dehydrogenase activity in 3T3-L1 adipocytes.

Persimmon peels, though usually discarded, are useful sources of nutraceuticals. In this study, persimmon peel-derived pomolic acid was found to suppress the increase in the activity of glycerol-3 phosphate dehydrogenase, a neutral fat synthesis-related enzyme, in 3T3-L1 adipocytes, whereas oleanolic and ursolic acids did not exert this effect. Therefore, persimmon peel may be an effective functional food material.

Oleanolic acid induces lipolysis and antioxidative activity in 3T3-L1 adipocytes

Oleanolic acid induces lipolysis and antioxidative activity in 3T3-L1 adipocytes

Indian Gooseberry and Barley Sprout Mixture Inhibits Adipogenesis and Lipogenesis Activity in 3T3-L1 Adipocytes

This study aimed to confirm the synergistic effect of an Indian gooseberry (IG) and barley sprout (BP) mixture in differentiated adipocytes. To this end, 3T3-L1 adipocytes were treated with IG, BP, and IGBP mixtures during the differentiation period. On the last day of differentiation, we measured intracellular cAMP, triglyceride (TG), and fatty acid (FA) levels, as well as performed Oil Red O staining, glycerol release, and Western blot assays. During adipogenesis, IGBP (200 μg/mL) increased the cAMP levels by more than 2-fold and decreased the protein expressions levels of p-CREB (66.3%), C/EBPα (79.4%), C/EBPβ (85.9%), and PPARγ (74.1%) compared to those in the C group. Furthermore, the expression levels of the adipogenesis-related genes and GLUT4 (more than 3-fold) were regulated. During lipogenesis, the IGBP (200 μg/mL) activated AMPK and ACC levels and reduced the protein expression levels of SREBP1c, FAS, and LPL. This reduced the FA and TG contents in the cells by 47.6% and 76.3%, respectively, compared to those in the differentiated control (C) group, resulting in a more than 5-fold increase in glycerol release. In conclusion, we found that IGBP inhibited TG synthesis during adipogenesis and lipogenesis, and thus, displayed potential as a functional health food for preventing obesity.

Effect of Astaxanthin on the Inhibition of Lipid Accumulation in 3T3-L1 Adipocytes via Modulation of Lipogenesis and Fatty Acid Transport Pathways.

Obesity is defined as a condition of excessive fat tissue accumulation. It was the major factor most closely associated with lifestyle-related diseases. In the present study, we investigated the effect of astaxanthin on the inhibition of lipid accumulation in 3T3-L1 adipocytes. 3T3-L1 adipocytes were treated with 0–25 µg/mL of astaxanthin for 0–48 h. The result indicated that astaxanthin significantly decreased the oil Red O stained material (OROSM), intracellular triglyceride accumulation, and glycerol 3-phosphate dehydrogenase (GPDH) activity in 3T3-L1 adipocytes (p < 0.05). At the molecular level, astaxanthin significantly down-regulated the mRNA expression of peroxisome proliferator-activated receptor-γ (PPARγ) in 3T3-L1 adipocytes (p < 0.05). Moreover, target genes of PPARγ on the inhibition of lipogenesis, such as Acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), fatty acid binding protein (aP2), cluster of differentiation 36 (CD36), and lipoprotein lipase (LPL) in 3T3-L1 adipocytes were significantly down-regulated at a time-dependent manner (p < 0.05). These results suggested that astaxanthin efficiently suppressed lipid accumulation in 3T3-L1 adipocytes and its action is associated with the down-regulation of lipogenesis-related genes and the triglyceride accumulation in 3T3-L1 adipocytes. Therefore, astaxanthin can be developed as a potential nutraceutical ingredient for the prevention of obesity in a niche market.

Two new nor-lignans from Selaginella pulvinata (Hook. & Grev.) Maxim and their antihyperglycemic activities

Two new nor-lignans, pulvin A (1) and moellenoside C (2), along with two known compounds (3–4) were isolated from the whole plant of Selaginella pulvinate (Hook. & Grev.) Maxim. The structures of the new compounds were established on the basis of spectroscopic data and acid hydrolysis. All the isolates were investigated for their antihyperglycemic activities in 3T3-L1 adipocytes. The results showed that compounds 1 and 2 promoted the glucose consumption prominently in 3T3-L1 adipocytes in a dose-response manner. Compound 1 and 2 induced 1.14–1.73 folds and 1.03–1.55 folds changes relative to the basal level, respectively, in the concentration range of 12.5 μM to 50 μM.

Astragalin, (3-O-glucoside of kaempferol), isolated from Moringa oleifera leaves modulates leptin, adiponectin secretion and inhibits adipogenesis in 3T3-L1 adipocytes

Inhibition of adipogenesis is crucial and is a key area of research to develop antiobesity drugs. In this study, 3-O-glucoside of kaempferol (astragalin) was isolated from Moringa oleifera leaves and evaluated for its lipolytic and antiadipogenic activity in 3T3-L1 adipocytes. Astragalin has substantially reduced the triglycerides content and lipid accumulation in 3T3-L1 adipocytes and enhanced the glycerol release in a dose dependent manner. The assay for secreted adipocytokines confirmed that, astragalin at a concentration of 20 µg/mL significantly (p < .01) increased the secretion of adiponectin, but decreased leptin secretion in 3T3-L1 adipocytes. In molecular studies, both the mRNA expression and corresponding protein expression of PPAR-γ, C/EBP-α, FAS, and leptin genes were downregulated while that of adiponectin was upregulated in astragalin treated groups. Taken together, astragalin of M. oleifera promotes lipolysis, suppresses adipogenesis in 3T3-L1 adipocytes, and may be considered as an effective candidate to treat obesity aliments.

MiR-210 in Exosomes Derived from Macrophages under High Glucose Promotes Mouse Diabetic Obesity Pathogenesis by Suppressing NDUFA4 Expression.

Objective Type 2 diabetes mellitus (T2DM) is featured by insulin resistance and lipid metabolism dysregulation. A large number of miRNAs were identified in exosomes derived from adipose tissue macrophages associated with T2DM pathogenesis, but its pathogenic roles remain unknown. This study is aimed at investigating the function of miR-210 in diabetic obesity. Methods Exosomes from mouse macrophage RAW264.7 cells were characterized by electron microscopy, combined with biomarker expression by western blot. Expression of miR-210 was determined by quantitative RT-PCR. Glucose uptake was measured by a fluorometric method, and the mitochondrial respiratory chain activity was evaluated by ELISA. The target gene of miR-210 was validated by dual-luciferase reporter and pull-down assays. A mouse obese diabetic model was established by a high-fat diet and streptozocin treatment. Results miR-210 was highly expressed in exosomes derived from high glucose-induced macrophage RAW264.7 cells. Macrophage-derived exosomes impaired glucose uptake and mitochondrial CIV complex activity and suppressed NADH dehydrogenase ubiquinone 1 alpha subcomplex 4 (NDUFA4) expression in 3T3-L1 adipocytes. miR-210 directly bind with mRNA sequences of NDUFA4 gene. Inhibition of miR-210 mitigated the effects of macrophage-derived exosomes on the glucose uptake and complex IV (CIV) activity in 3T3-L1 adipocytes, and NDUFA4 overexpression offset the inhibition of glucose uptake and CIV activity by macrophage-derived exosomes. Furthermore, mice with miR-210 knockout showed greatly repressed diabetic obesity development. Conclusion miR-210 derived from adipose tissue macrophages promotes mouse obese diabetes pathogenesis by regulating glucose uptake and mitochondrial CIV activity through targeting NDUFA4 gene expression.

Mulberry Fruit Extract Ameliorates Adipogenesis via Increasing AMPK Activity and Downregulating MicroRNA-21/143 in 3T3-L1 Adipocytes.

Mulberry (Morus alba L.) fruits have long been used in traditional medicine and as edible berries in many countries. This study investigated the antiadipogenic effect of high hydrostatic pressure mulberry fruit extract (MFE) during 3T3-L1 adipocyte differentiation. MFE decreased lipid and triglyceride accumulation and glycerol-3-phosphate dehydrogenase activity. The mRNA expression levels of genes related to adipogenesis, such as the adipocyte protein 2, proliferator-activated receptor-γ, and CCAAT/enhancer binding protein-α, were suppressed by MFE. They also reduced microRNA (miR)-21 and miR-143 expression, which are involved in adipogenesis. In contrast, adenosine monophosphate-activated protein kinase (AMPK) activity was increased by MFE. These results suggested that MFE may suppress adipogenesis through modulating miR-21/143 expression and AMPK activity in 3T3-L1 adipocytes, which may be useful as antiobesity food agents.

Intracellular cAMP contents regulate NAMPT expression via induction of C/EBPβ in adipocytes

A decline in intracellular nicotinamide adenine mononucleotide (NAD+) causes adipose tissue dysfunction. Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in the NAD+ biosynthesis pathway. However, the molecular mechanism that mediates regulation of NAMPT expression in adipocytes is yet to be elucidated. This study found that intracellular cAMP regulates NAMPT expression and promoter activity in 3T3-L1 adipocytes. cAMP-mediated Nampt promoter activity was suppressed by protein kinase A inhibitor H89, whereas AMP-activated protein kinase inhibitor compound C did not affect cAMP-mediated Nampt promoter activity. Intracellular cAMP induced CCAAT/enhancer-binding protein β (C/EBPβ) expression. Knockdown of C/EBPβ suppressed NAMPT expression and promoter activity. Furthermore, the Nampt promoter was activated by C/EBPβ, while LIP activated the dominant-negative form of C/EBPβ. Promoter sequence analysis revealed that the region from −96 to −76 on Nampt was required for C/EBPβ-mediated promoter activity. Additionally, chromatin immunoprecipitation assay demonstrated that C/EBPβ was bound to the promoter sequences of Nampt. Finally, NAMPT inhibitor FK866 suppressed adipogenesis in 3T3-L1 cells, and this suppressive effect was restored by nicotinamide mononucleotide treatment. These findings showed that intracellular cAMP increased NAMPT levels by induction of C/EBPβ expression and indicated that the induction of NAMPT expression was important for adipogenesis.

Phenolic compounds from coffee by-products modulate adipogenesis-related inflammation, mitochondrial dysfunction, and insulin resistance in adipocytes, via insulin/PI3K/AKT signaling pathways

The aim of this study was to evaluate the inhibitory potential of aqueous extracts from coffee silverskin (CSE) and husk (CHE) and their main phenolics on adipogenesis, obesity-related inflammation, mitochondrial dysfunction, and insulin resistance, in vitro. Coffee by-products extracts (31–500 μg mL−1) and pure phenolics (100 μmol L−1) reduced lipid accumulation and increased mitochondrial activity in 3T3-L1 adipocytes. Also reduced the expression of inducible nitric oxide synthase and cyclooxygenase-2 and diminished secretion of pro-inflammatory factors in LPS-stimulated RAW2643.7 macrophages. Cytokine release diminished (tumor necrosis factor α: 23–57%; monocyte chemoattractant protein 1: 42–60%; interleukin-6: 30–39%) and adiponectin increased (7–13- fold) in adipocytes treated with macrophage-conditioned media. ROS scavenging and activation of peroxisome proliferator-activated receptor γ coactivator 1-α pathway counteracted mitochondrial dysfunction. Increases in insulin receptor (1.4 to 4-fold), phosphoinositide 3-kinase (2 to 3-fold) and protein kinase B (1.3 to 3-fold) phosphorylation, in conjunction with a decrease in serine phosphorylation of insulin receptor substrate 1, evoked glucose transporter 4 translocation (8–15-fold) and glucose uptake (44–85%). CSE and CHE phenolics inhibited adipogenesis and elicited adipocytes browning. Suppressing macrophages-adipocytes interaction alleviated inflammation-triggered mitochondrial dysfunction and insulin resistance. CSE and CHE are beneficial in reducing adipogenesis and inflammation-related disorders.

Laser Photobiomodulation 904 nm Promotes Inhibition of Hormone-Sensitive Lipase Activity in 3T3-L1 Adipocytes Differentiated Cells.

Background: The lipid metabolism is essential for maintaining the body's energy responses. Laser photobiomodulation triggers many important cellular effects, but these effects on lipid metabolism are not well described. In this study, we analyzed the laser photobiomodulation in the hormone-sensitive lipase (HSL) activity, a key enzyme in the triglycerides (TAG) hydrolysis in adipose tissue 3T3-L1. Methods: Cells were submitted to the differentiation protocol in adipose cells, irradiated with 1, 2, and 3J with laser (904 nm-60 mw-laser diode) and incubated for 4 h after irradiation. Results: The response of laser photobiomodulation was able to trigger an inhibition of HSL activity (control = 0.057 ± 0.0008; 1J = 0.050 ± 0.0003; 2J = 0.0477 ± 0.002; 3J = 0.051 ± 0.002; p = 0.0003 against the control), but no modulation was observed in TAG levels into the medium (control = 26.5856 ± 0.52; 1J = 26.5856 ± 0.52; 2J = 27.2372 ± 1.41; 3J = 25.9991 ± 0.1303; p = 0.18). Conclusions: This is the first study of HSL activity modulation with laser radiation, suggesting that photobiomodulation can influence adipose tissue metabolism and open a new field of study.

Improvement of high-glucose and insulin resistance of chromium malate in 3T3-L1 adipocytes by glucose uptake and insulin sensitivity signaling pathways and its mechanism.

Previous study has revealed that chromium malate could improve insulin resistance and the regulation of fasting blood glucose in type 2 diabetic rats. This study was designed to investigate the effect of chromium malate on hypoglycemic and improve insulin resistance activities in 3T3-L1 adipocytes with insulin resistance and investigate the acting mechanism. The result indicated that chromium malate exhibited direct hypoglycemic activity in vitro. Compared with the model group, chromium malate could significantly promote the expression levels of GLUT-4, Akt, Irs-1, PPARγ, PI3K and p38-MAPK and their mRNA, increase p-AKT/AKT level, AKT and AMPKβ1 phosphorylation and reduce Irs-1 phosphorylation and p-Irs-1/Irs-1 level in 3T3-L1 adipocytes (p < 0.05). Chromium malate is more effective in regulating the proteins and mRNA expressions than those of chromium trichloride and chromium picolinate. Compared to the model group, pretreatment with the specific p38-MAPK inhibitor completely inhibited the GLUT-4 and Irs-1 proteins and mRNA expressions induced by the chromium malate. In conclusion, chromium malate had a beneficial influence on improvement of controlling glucose levels and insulin resistance in 3T3-L1 adipocytes with insulin resistance by regulating proteins productions and genes expressions in glucose uptake and insulin sensitivity signaling pathways.

Three New Polyacetylene Glycosides from the Roots of Heracleum dissectum and Their Triglyceride Accumulating Activities in 3T3-L1 Cells.

Continually phytochemical study of the roots of Heracleum dissectum had led to the isolation of three previously undescribed polyacetylene glycosides (1-3), together with seven known compounds, including one polyacetylene (8) and six coumarins (4-7 and 9-10) using diverse chromatographic methods. The structures of these three new compounds were characterized and identified as deca-4,6-diyn-1-yl β-d-glucopyranosyl-(1→6)-β-d-glucopyranosyl-(1→2)-β-d-glucopyranoside (1), (8Z)-dec-8-ene-4,6-diyn-1-yl β-d-glucopyranosyl-(1→6)-β-d-glucopyranosyl-(1→2)-β-d-glucopyranoside (2), and (8E)-dec-8-ene-4,6-diyn-1-yl β-d-glucopyranosyl-(1→6)-β-d-glucopyranosyl-(1→2)-β-d-glucopyranoside (3) based on their physicochemical properties and extensive analyses of various spectroscopic data. Their triglycerides accumulating activities were assayed and the results showed that the three new polyacetylene glycosides (1-3) exhibited triglyceride accumulating activities in 3T3-L1 adipocytes.

Inflammation stimulates hypoxia-inducible factor-1α regulatory activity in 3T3-L1 adipocytes with conditioned medium from lipopolysaccharide-activated RAW 264.7 macrophages.

Obesity is a multifactorial, chronic, inflammatory disease that involves different processes, such as adipose tissue hypoxia. The aim of the current study was to characterize the effects of conditioned medium (CM) from lipopolysaccharide (LPS)-activated macrophages on the regulation of hypoxia-inducible factor 1α (HIF-1α)-related genes in murine adipocytes. For the in vitro analyses, 3T3-L1 murine adipocytes (9 days postdifferentiation) were incubated either in CM (25% medium of RAW 264.7 murine macrophages with 24 hr 500 ng/ml LPS), LPS at 500 ng/ml, or hypoxia (Hx; 1% O2 , 94% N2 , 5% CO2 ) for 24 hr. For the in vivo experiments, mice were fed a high-fat diet. Both epididymal white adipose tissue (eWAT) and adipocytes in CM showed upregulation of Glut1, Mcp1, Il10, Tnf, and Il1b. The secretion of IL-6, TNF-α, and MCP-1 was also increased in CM-treated adipocytes. Moreover, increased levels of HIF-1α subunit and nuclear factor kappa B p65 were found after CM treatment, linking Hx, and inflammation. HIF-1α directly bound vascular endothelial growth factor A (Vegfa) and uncoupling protein 2 (Ucp2) genes, up- and downregulating its expression, respectively. Furthermore, the oxygen consumption rate was 30% lower in CM. The siRNA knockdown of mammalian target of rapamycin (Mtor) reversed the induction of HIF-1α found in CM. The macrophage infiltration simulated through CM seems to be a similar environment to an abnormally enlarged eWAT. We have evidenced that HIF-1α plays a regulatory role in the expression of Vegfa and Ucp2 in CM. Finally, the inhibition of the mTOR pathway prevented the HIF-1α activation induced by CM. The involvement of HIF-1α under proinflammatory conditions provides insight into the origins of Hx in obesity.

The Inhibitory Effects of Djulis (Chenopodium formosanum) and Its Bioactive Compounds on Adipogenesis in 3T3-L1 Adipocytes.

The aim of this study was to provide new insights into the role of the ethanolic extracts of Djulis (Chenopodium formosanum, EECF) and its bioactive compounds in preventing adipogenesis in 3T3-L1 adipocytes. The results demonstrated EECF significantly inhibited oil red O-stained material (OROSM), triglyceride levels and glycerol-3-phosphate dehydrogenase (GPDH) activity in 3T3-L1 adipocytes. The expression of the critical molecules involved in lipid synthesis such as PPARγ, C/EBPα and SREBP-1c was attenuated in EECF-treated cells. According to HPLC-DAD and HPLC-MS/MS analysis, rutin, kaempferol, betanin and another nine compounds were present in EECF. The suppression of lipid accumulation by rutin, kaempferol and betanin occurred by decreasing the gene expression of PPARγ, C/EBPα and SREBP-1c. Taken together, these findings suggest the presence of bioactive compounds in EECF may partly account for the anti-adipogenesis of EECF and EECF is therefore a potentially lipid lowering functional food.

Deep Sea Water Improves Abnormalities in Lipid Metabolism through Lipolysis and Fatty Acid Oxidation in High-Fat Diet-Induced Obese Rats.

Deep sea water (DSW) is a natural marine resource that has been utilized for food, agriculture, cosmetics, and medicine. The aim of this study was to investigate whether DSW has beneficial lipid metabolic effects in an animal model. Our previous in vitro study indicated that DSW significantly decreased the intracellular triglyceride and glycerol-3-phosphate dehydrogenase activity in 3T3-L1 adipocytes. DSW also inhibited the gene levels of adipocyte differentiation, lipogenesis, and adipocytokines, and up-regulated gene levels of lipolysis and fatty acid oxidation. In the present study, the results showed that body weight, liver, adipose tissue, hepatic triglycerides and cholesterol, and serum parameters in the high-fat diet (HFD) + DSW groups were significantly lower compared to the HFD group. Moreover, the fecal output of total lipids, triglycerides, and cholesterol in the HFD + DSW groups was significantly higher than that of the HFD group. Regarding gene expression, DSW significantly increased the gene levels of lipolysis and fatty acid oxidation, and decreased the gene levels of adipocytokine in the adipose tissue of rats with HFD-induced obesity. These results indicate a potential molecular mechanism by which DSW can suppress obesity in rats with HFD-induced obesity through lipolysis and fatty acid oxidation.