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1
Vasileva, Liliya, Martina Savova, Daniel Tews, Martin Wabitsch, and Milen Georgiev. "Rosmarinic acid attenuates obesity and obesity-related inflammation in human adipocytes." Food and Chemical Toxicology 149 (January 19, 2021): 112002. https://doi.org/10.1016/j.fct.2021.112002.
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Chronic low-grade inflammation is a hallmark of obesity and its related metabolic disorders. At the same time signaling from pro-inflammatory factors such as transforming growth factor beta (TGF-β) or interleukin 17A (IL- 17A) are proposed as crucial for the commitment of fibroblast progenitor cells towards adipogenic differentiation. Modulation of inflammation during adipogenic differentiation is incompletely explored as a potential approach to prevent metabolic disorders. Rosmarinic acid (RA) is a caffeic acid derivative known for its antiinflammatory effects. Experimental studies of its activity on adipogenic factors or in vivo obesity models are, however, controversial and hence insufficient. Here, we investigated the anti-adipogenic action of RA in human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes. Gene expression levels of key players in adipogenesis and lipid metabolism were assessed. Furthermore, a molecular mechanism of action was proposed. The most prominent effect was found on the translation of C/EBPα, PPARγ and adiponectin, as well as on the modulation of TGF1B and IL17A. Interestingly, involvement of NRF2 signaling was identified upon RA treatment. In summary, our findings indicate that RA prevents inflammation and excessive lipid accumulation in human adipocytes. Data from the molecular analysis demonstrate that RA has potential for treatment of obesity and obesityrelated inflammation.
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Oh, Jung Hwan, Fatih Karadeniz, Mi-Soon Jang, Hojun Kim, Youngwan Seo та Chang-Suk Kong. "Loliolide from Artemisia princeps Suppresses Adipogenesis in Human Bone Marrow-Derived Mesenchymal Stromal Cells via Activation of AMPK and Wnt/β-catenin Pathways". Applied Sciences 11, № 12 (2021): 5435. http://dx.doi.org/10.3390/app11125435.
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Regulating the adipogenic differentiation mechanism is a valid and promising mechanism to battle obesity. Natural products, especially phytochemicals as nutraceuticals, are important lead molecules with significant activities against obesity. Loliolide is a monoterpenoid hydroxyl lactone found in many dietary plants. The effect of loliolide on adipogenic differentiation is yet to be determined. Therefore, the present study aimed to evaluate its anti-adipogenic potential using human bone marrow-derived mesenchymal stromal cells (hBM-MSCs) and assess its mechanism of action. Adipo-induced hBM-MSCs were treated with or without loliolide and their adipogenic characteristics were examined. Loliolide treatment decreased the lipid accumulation and expression of adipogenic transcription factors, PPARγ, C/EBPα, and SREBP1c. Adipo-induced hBM-MSCs also displayed increased AMPK phosphorylation and suppressed MAPK activation following loliolide treatment according to immunoblotting results. Importantly, loliolide could stimulate Wnt10b expression and active β-catenin translocation to exert PPARγ-linked adipogenesis suppression. In conclusion, loliolide was suggested to be a potential anti-adipogenic agent which may be utilized as a lead compound for obesity treatment or prevention.
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Gautam, Jyoti, Vikram Khedgikar, Priyanka Kushwaha та ін. "Formononetin, an isoflavone, activates AMP-activated protein kinase/β-catenin signalling to inhibit adipogenesis and rescues C57BL/6 mice from high-fat diet-induced obesity and bone loss". British Journal of Nutrition 117, № 5 (2017): 645–61. http://dx.doi.org/10.1017/s0007114517000149.
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AbstractBalance between adipocyte and osteoblast differentiation is the key link of disease progression in obesity and osteoporosis. We have previously reported that formononetin (FNT), an isoflavone extracted from Butea monosperma, stimulates osteoblast formation and protects against postmenopausal bone loss. The inverse relationship between osteoblasts and adipocytes prompted us to analyse the effect of FNT on adipogenesis and in vivo bone loss, triggered by high-fat diet (HFD)-induced obesity. The anti-obesity effect and mechanism of action of FNT was determined in 3T3-L1 cells and HFD-induced obese male mice. Our findings show that FNT suppresses the adipogenic differentiation of 3T3-L1 fibroblasts, through down-regulation of key adipogenic markers such as PPARγ, CCAAT/enhancer-binding protein alpha (C/EBPα) and sterol regulatory element-binding protein (SREBP) and inhibits intracellular TAG accumulation. Increased intracellular reactive oxygen species levels and AMP-activated protein kinase (AMPK) activation accompanied by stabilisation of β-catenin were attributed to the anti-adipogenic action of FNT. In vivo, 12 weeks of FNT treatment inhibited the development of obesity in mice by attenuating HFD-induced body weight gain and visceral fat accumulation. The anti-obesity effect of FNT results from increased energy expenditure. FNT also protects against HFD-induced dyslipidaemia and rescues deterioration of trabecular bone volume by increasing bone formation and decreasing bone resorbtion caused by HFD. FNT’s rescuing action against obesity-induced osteoporosis commenced at the level of progenitors, as bone marrow progenitor cells, obtained from the HFD mice group supplemented with FNT, showed increased osteogenic and decreased adipogenic potentials. Our findings suggest that FNT inhibits adipogenesis through AMPK/β-catenin signal transduction pathways and protects against HFD-induced obesity and bone loss.
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Mladenova, Saveta, Martina Savova, Andrey Marchev та ін. "Anti-adipogenic activity of maackiain and ononin is mediated via inhibition of PPARγ in human adipocytes". Biomedicine & Pharmacotherapy 149 (1 квітня 2022): 112908. https://doi.org/10.1016/j.biopha.2022.112908.
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Obesity is a global health burden for which we do not yet have effective treatments for prevention or therapy. Plants are an invaluable source of bioactive leads possessing anti-adipogenic potential. Ethnopharmacological use of Ononis spinosa L. roots (OSR) for treatment of obesity and metabolic disorders requires а scientific rationale. The current study examined the anti-adipogenic capacity of OSR and its secondary metabolites ononin (ONON) and maackiain (MACK) in human adipocytes as an in vitro model of obesity. Both ONON and MACK diminished lipid accumulation during adipocyte differentiation. Molecular docking analysis exposed the potential interactions between MACK or ONON and target regulatory adipogenic proteins. Furthermore, results from an RT-qPCR analysis disclosed significant upregulation of AMPK by MACK and ONON treatment. In addition, ONON increased SIRT1, PI3K and ACC mRNA expression, while MACK notably downregulated CEBPA, AKT, SREBP1, ACC and ADIPOQ. The protein level of PI3K, C/EBPα, PPARγ and adiponectin was reduced upon MACK treatment in a concentration-dependent manner. Similarly, ONON suppressed PI3K, PPARγ and adiponectin protein abundance. Finally, our study provides evidence that ONON exerts anti-adipogenic effect by upregulation of SIRT1 and inhibition of PI3K, PPARγ and adiponectin, while MACK induced strong inhibitory effect on adipogenesis via hampering PI3K, PPARγ/C/EBPα signaling and anti-lipogenic effect through downregulation of SREBP1 and ACC. Even though OSR does not hamper adipogenic differentiation, it could be exploited as a source of natural leads with anti-adipogenic potential. The multidirectional mechanism of action of MACK warrant further validation in the context of in vivo obesity models.
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Lee, Jung Im, Jung Hwan Oh, Fatih Karadeniz, Chang-Suk Kong, and Youngwan Seo. "Inhibitory Effects of Sesquiterpenoids Isolated from Artemisia scoparia on Adipogenic Differentiation of 3T3-L1 Preadipocytes." International Journal of Molecular Sciences 25, no. 1 (2023): 200. http://dx.doi.org/10.3390/ijms25010200.
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Obesity and related complications are significant health issues in modern society, largely attributed to a sedentary lifestyle and a carbohydrate-rich diet. Since anti-obesity drugs often come with severe side effects, preventative measures are being sought globally, including dietary changes and functional foods that can counteract weight gain. In this context, plant-based metabolites are extensively studied for their advantageous biological effects against obesity. Several plants within the Artemisia genus have been reported to possess anti-adipogenic properties, preventing adipocytes from maturing and accumulating lipids. The present study investigated the anti-adipogenic potential of two sesquiterpenoids, reynosin and santamarine, isolated from A. scoparia in adipose-induced 3T3-L1 preadipocytes. Differentiating 3T3-L1 adipocytes treated with these isolated compounds displayed fewer adipogenic characteristics compared to untreated mature adipocytes. The results indicated that cells treated with reynosin and santamarine accumulated 55.0% and 52.5% fewer intracellular lipids compared to untreated control adipocytes, respectively. Additionally, the mRNA expression of the key adipogenic marker, transcription factor PPARγ, was suppressed by 87.2% and 91.7% following 60 μM reynosin and santamarine treatment, respectively, in differentiated adipocytes. Protein expression was also suppressed in a similar manner, at 92.7% and 82.5% by 60 μM reynosin and santamarine treatment, respectively. Likewise, SERBP1c and C/EBPα were also downregulated at both gene and protein levels in adipocytes treated with samples during differentiation. Further analysis suggested that the anti-adipogenic effect of the compounds might be a result of AMPK activation and the subsequent suppression of MAPK phosphorylation. Overall, the present study suggested that sesquiterpenoids, reynosin, and santamarine were two potential bioactive compounds with anti-adipogenic properties. Further research is needed to explore other bioactive agents within A. scoparia and elucidate the in vivo action mechanisms of reynosin and santamarine.
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Ono, Tomoji, Satoru Morishita, Chikako Fujisaki, et al. "Effects of pepsin and trypsin on the anti-adipogenic action of lactoferrin against pre-adipocytes derived from rat mesenteric fat." British Journal of Nutrition 105, no. 2 (2010): 200–211. http://dx.doi.org/10.1017/s0007114510003259.
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Lactoferrin (LF) is a multifunctional glycoprotein in mammalian milk. In a previous report, we showed that enteric-coated bovine LF tablets can decrease visceral fat accumulation, hypothesising that the enteric coating is critical to the functional peptides reaching the visceral fat tissue and exerting their anti-adipogenic activity. The aim of the present study was to assess whether ingested LF can retain its anti-adipogenic activity. We therefore investigated the effects of LF and LF treated with digestive enzymes (the stomach enzyme pepsin and the small intestine enzyme trypsin) on lipid accumulation in pre-adipocytes derived from the mesenteric fat tissue of male Sprague–Dawley rats. Lipid accumulation in pre-adipocytes was significantly reduced by LF in a dose-dependent manner and was associated with reduction in gene expression of CCAAT/enhancer binding protein delta, CCAAT/enhancer binding protein alpha and PPARγ as revealed by DNA microarray analysis. Trypsin-treated LF continued to show anti-adipogenic action, whereas pepsin-treated LF abrogated the activity. When an LF solution (1000 mg bovine LF) was administered by gastric intubation to Sprague–Dawley rats, immunoreactive LF determined by ELISA could be detected in mesenteric fat tissue at a concentration of 14·4 μg/g fat after 15 min. The overall results point to the importance of enteric coating for action of LF as a visceral fat-reducing agent when administered in oral form.
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Kim, Nari, Sekyung Lee, Eun-Jin Jung та ін. "Yeast-Hydrolysate-Derived 1-Methyl-1,2,3,4-tetrahydro-β-carboline-3-carboxylic Acid Inhibits Fat Accumulation during Adipocyte Differentiation". Foods 12, № 18 (2023): 3466. http://dx.doi.org/10.3390/foods12183466.
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This study aimed to investigate the impact of yeast hydrolysate (YH) on lipogenesis, elucidate its mechanistic action, and identify the active compounds responsible for its anti-adipogenic effects. YH (2 mg/mL) significantly reduced Oil Red O-stained lipids. YH (2 mg/mL) also downregulated C/EBPβ and upregulated KLF2, both of which are early adipogenic factors. Moreover, YH (2 mg/mL) decreased C/EBPα, PPARγ, FABP4, FAS, ACC, and HMGCR mRNA expression. Additionally, YH significantly downregulated SEBP1c and SREBP2 and their target genes, which govern fatty acid and cholesterol metabolism; however, 2 mg/mL YH had a greater suppressive effect on SREBP1c than on SREBP2. YH (2 mg/mL) also significantly reduced the mRNA level of G6PD and malic enzyme, which are enzymes that synthesize NADPH for lipid synthesis, compared with the control. Furthermore, 1-methyl-1,2,3,4-tetrahydro-β-carboline-3-carboxylic acid (MTCA) was identified as the active compound with anti-adipogenic effects using solvent fractionation and chromatographic analysis of YH, and 1.1 μg/mL MTCA significantly downregulated SREBP1c/SREBP2 mRNAs by 47.8% and 69.2%, respectively, along with the target genes FAS, ACC, and HMGCR by 79.0%, 77.0%, and 40.9%, respectively. Collectively, YH effectively suppressed adipogenic lipid storage by downregulating SREBP- and NADPH-synthesizing genes. These findings suggest that YH containing MTCA has the potential to act as an anti-obesity agent.
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Mladenova, Saveta, Liliya Vasileva, Martina Savova, et al. "Anti-Adipogenic Effect of Alchemilla monticola is Mediated Via PI3K/AKT Signaling Inhibition in Human Adipocytes." Frontiers in Pharmacology 12 (August 18, 2021): 707507. https://doi.org/10.3389/fphar.2021.707507.
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Obesity is a persistent and continuously expanding social health concern. Excessive fat mass accumulation is associated with increased risk of chronic diseases including diabetes, atherosclerosis, non-alcoholic steatohepatitis, reproductive dysfunctions and certain types of cancer. <em>Alchemilla monticola</em> Opiz. is a perennial plant of the Rosaceae family traditionally used to treat inflammatory conditions and as a component of weight loss herbal mixtures. In the search for bioactive leads with potential anti-adipogenic effect from <em>A. monticola</em> extract (ALM), we have employed nuclear magnetic resonance (NMR) based metabolomics to obtain data for the phytochemical profile of the extract. Further, molecular docking simulation was performed against key adipogenic targets for selected pure compounds, present in the ALM extract. Evaluation of the biological activity was done in human adipocytes exposed to ALM (5, 10 and 25 μg/ml), pure astragalin (AST) or quercitrin (QUE) both at the concentrations of 5, 10 and 25 μM. Investigation of the molecular pathways involved was performed through real-time quantitative PCR and Western blot analyses. According to the docking predictions strong putative affinity was revealed for both AST and QUE towards peroxisome proliferator-activated receptor gamma (PPARγ) and phosphoinositide 3-kinase (PI3K). Assessment of the intracellular lipid accumulation revealed anti-adipogenic activity of ALM. Correspondingly, the expression of the adipogenic genes CCAAT/enhancer-binding protein alpha (<em>CEBPA</em>) and <em>PPARG</em> was downregulated upon ALM and AST treatment. The Western blotting results exposed protein kinase B (AKT), PI3K and PPARγ as targets for the inhibitory effect of ALM and AST on adipogenesis. Collectively, we provide a broader insight of the phytochemical composition of <em>A. monticola</em>. Additionally, we demonstrate the anti-adipogenic effect of ALM and its active compound AST in human adipocytes. Furthermore, PI3K/AKT signaling pathway is identified to mediate the ALM anti-adipogenic action. Hence, the ALM extract and its secondary metabolite AST are worth further exploration as potentially active agents in obesity management.
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Yadav, Anil Kumar, and Byeong-Churl Jang. "Anti-adipogenic and Pro-lipolytic Effects on 3T3-L1 Preadipocytes by CX-4945, an Inhibitor of Casein Kinase 2." International Journal of Molecular Sciences 23, no. 13 (2022): 7274. http://dx.doi.org/10.3390/ijms23137274.
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Casein kinase 2 (CK2) is a ubiquitously expressed serine/threonine kinase and is upregulated in human obesity. CX-4945 (Silmitasertib) is a CK2 inhibitor with anti-cancerous and anti-adipogenic activities. However, the anti-adipogenic and pro-lipolytic effects and the mode of action of CX-4945 in (pre)adipocytes remain elusive. Here, we explored the effects of CX-4945 on adipogenesis and lipolysis in differentiating and differentiated 3T3-L1 cells, a murine preadipocyte cell line. CX-4945 at 15 μM strongly reduced lipid droplet (LD) accumulation and triglyceride (TG) content in differentiating 3T3-L1 cells, indicating the drug’s anti-adipogenic effect. Mechanistically, CX-4945 reduced the expression levels of CCAAT/enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and perilipin A in differentiating 3T3-L1 cells. Strikingly, CX-4945 further increased the phosphorylation levels of cAMP-activated protein kinase (AMPK) and liver kinase B-1 (LKB-1) while decreasing the intracellular ATP content in differentiating 3T3-L1 cells. In differentiated 3T3-L1 cells, CX-4945 had abilities to stimulate glycerol release and elevate the phosphorylation levels of hormone-sensitive lipase (HSL), pointing to the drug’s pro-lipolytic effect. In addition, CX-4945 induced the activation of extracellular signal-regulated kinase-1/2 (ERK-1/2), and PD98059, an inhibitor of ERK-1/2, attenuated the CX4945-induced glycerol release and HSL phosphorylation in differentiated 3T3-L1 cells, indicating the drug’s ERK-1/2-dependent lipolysis. In summary, this investigation shows that CX-4945 has strong anti-adipogenic and pro-lipolytic effects on differentiating and differentiated 3T3-L1 cells, mediated by control of the expression and phosphorylation levels of CK2, C/EBP-α, PPAR-γ, FAS, ACC, perilipin A, AMPK, LKB-1, ERK-1/2, and HSL.
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Dhok, Mayuri, Avinash Kharat, Ramesh Bhonde, and Nilima Ghangale. "Evidence based Osteogenic, anti adipogenic and anti- senescence action of Centella asiatica extract on Dental pulp stem cells." International Journal of Ayurvedic Medicine 15, no. 3 (2024): 684–88. http://dx.doi.org/10.47552/ijam.v15i3.4879.
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Aim: Centella asiatica linn family of Apiaceae has been used as a traditional medicine as anti-aging remedy to minimize the severity of aging problems. However the effects of Centella asiatica on stem cell differentiation and anti-aging activity are not fully understood. In this investigation we tested the effect of an aqueous extract of Centella asiatica on senescence and osteogenic, chondrogenic and adipogenic differentiation of human dental pulp stem cells ( hDPSCs). Methods: DPSC (n = 10) from the human pulp was treated with various concentrations of Centella asiatica(CA). The cytotoxicity of CA assessed using the MTT. The hDPSCs were then induced to osteogenic, chondrogenic, and adipogenic differentiation for 6 and 21 days using either CA alone or a combination of Centella asiatica with an appropriate induction media. We also evaluated the early and late passage senescence activity of DPSC. Key finding: Our data demonstrate effect of CA extract on adipogenesis, chondrogenesis and osteogenesis, and anti-aging activity. We found that there was initial increase in adipogenesis which was diminished in long-term culture. Similarly, the extract was found to enhance chondrogenesis and osteogenesis and reduced senescence as revealed by β-galactosidase staining. Significance: The present study demonstrated for the first time that the CA extract was able to inhibit adipogenesis, senescence, and accelerated osteogenesis in DPSCs. Overall results show that CA (Mandukaparni) extract can be used to treat osteoporosis, delay aging and reduce obesity.
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Kim, Jong-Yeon, Eun-Jung Park, and Hae-Jeung Lee. "Ameliorative Effects of Lactobacillus plantarum HAC01 Lysate on 3T3-L1 Adipocyte Differentiation via AMPK Activation and MAPK Inhibition." International Journal of Molecular Sciences 23, no. 11 (2022): 5901. http://dx.doi.org/10.3390/ijms23115901.
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Lactobacillus plantarum HAC01 has been shown to effectively treat metabolic diseases. However, the precise pharmacological effects and molecular mechanisms of L. plantarum HAC01 remain unclear. In this study, we investigate the anti-adipogenic effects of L. plantarum HAC01 lysate and its associated mechanism of action. To induce lipid accumulation, 3T3-L1 cells were incubated in differentiation media with or without L. plantarum HAC01 lysate. Our results show that L. plantarum HAC01 lysate treatment not only reduced lipid accumulation during the differentiation of 3T3-L1 cells, but also decreased the expression of adipogenic and lipogenic genes involved in lipid metabolism in a dose-dependent manner. Additionally, L. plantarum HAC01 lysate inhibited CCAAT/enhancer-binding protein (C/EBP) beta within 4 h of differentiation induction and inhibited peroxisome proliferator-activated receptor gamma, C/EBP alpha, and sterol regulatory element-binding proteins within 2 d. Moreover, treatment with L. plantarum HAC01 lysate increased the phosphorylation of adenosine monophosphate-activated protein kinase, an important regulator of energy metabolism, and decreased the phosphorylation of mitogen-activated protein kinase. These results indicate that L. plantarum HAC01 lysate may have anti-adipogenic effects and support its potential as a useful agent for the treatment of obesity.
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Karadeniz, Fatih, Jung Hwan Oh, Mi Soon Jang, Youngwan Seo, and Chang-Suk Kong. "Libanoridin Isolated from Corydalis heterocarpa Inhibits Adipogenic Differentiation of Bone Marrow-Derived Mesenchymal Stromal Cells." International Journal of Molecular Sciences 24, no. 1 (2022): 254. http://dx.doi.org/10.3390/ijms24010254.
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Bone marrow adiposity is a complication in osteoporotic patients. It is a result of the imbalance between adipogenic and osteogenic differentiation of bone marrow cells. Phytochemicals can alleviate osteoporotic complications by hindering bone loss and decreasing bone marrow adiposity. Corydalis heterocarpa is a biennial halophyte with reported bioactivities, and it is a source of different coumarin derivatives. Libanoridin is a coumarin isolated from C. heterocarpa, and the effect of libanoridin on adipogenic differentiation of human bone marrow-derived mesenchymal stromal cells (hBM-MSCs) was evaluated in the present study. Cells were induced to undergo adipogenesis, and their intracellular lipid accumulation and expression of adipogenic markers were observed under libanoridin treatment. Results showed that 10 μM libanoridin-treated adipocytes accumulated 44.94% less lipid compared to untreated adipocytes. In addition, mRNA levels of PPARγ, C/EBPα, and SREBP1c were dose-dependently suppressed with libanoridin treatment, whereas only protein levels of PPARγ were decreased in the presence of libanoridin. Fluorescence staining of adipocytes also revealed that cells treated with 10 μM libanoridin expressed less PPARγ compared to untreated adipocytes. Protein levels of perilipin and leptin, markers of mature adipocytes, were also suppressed in adipocytes treated with 10 μM libanoridin. Analysis of MAPK phosphorylation levels showed that treatment with libanoridin inhibited the activation of p38 and JNK MAPKs observed by decreased levels of phosphorylated p38 and JNK protein. It was suggested that libanoridin inhibited adipogenic differentiation of hBM-MSCs via suppressing MAPK-mediated PPARγ signaling. Future studies revealing the anti-adipogenic effects of libanoridin in vivo and elucidating its action mechanism will pave the way for libanoridin to be utilized as a nutraceutical with anti-osteoporotic properties.
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Kim, Ji Hye, Mi Jeong Jo, Hye Jin Go, Nam Gyu Park, and Gun Do Kim. "Anti-adipogenic effect of mastoparan B analogue peptide on 3T3-L1 preadipocytes." Bangladesh Journal of Pharmacology 13, no. 4 (2018): 333–39. http://dx.doi.org/10.3329/bjp.v13i4.37351.
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Mastoparan B (MP-B), a cationic tetradecapeptide isolated from the venom of the Vespa basalis, exhibits cardiovascular effects, local edema and antibacterial activity. In this study, the anti-adipogenic effect of an MP-B analogue and its mechanism of action in 3T3-L1 preadipocytes were studied. The MP-B analogue (MP-B12) inhibited preadipocyte differentiation and decreased the expression of adipogenic transcription factors, including CCAAT/enhancer binding protein-alpha (C/EBPα), nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) and sterol regulatory element-binding protein-1 (SREBP-1). Moreover, MP-B12 regulated the phosphorylation of Akt and glycogen synthase kinase-3 beta (GSK-3β), both of which play a role in preadipocyte differentiation, in which insulin and certain growth factors stimulated adipogenesis. This study demonstrates that MP-B12 inhibits preadipocyte differentiation and the accumulation of lipid droplets in 3T3-L1 preadipocytes and could potentially be used to treat obesity.Video Clip of Methodology:4 min 11 sec Full Screen Alternate
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Chayaratanasin, Poramin, Allen Caobi, Chaturong Suparpprom, et al. "Clitoria ternatea Flower Petal Extract Inhibits Adipogenesis and Lipid Accumulation in 3T3-L1 Preadipocytes by Downregulating Adipogenic Gene Expression." Molecules 24, no. 10 (2019): 1894. http://dx.doi.org/10.3390/molecules24101894.
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Clitoria ternatea (commonly known as blue pea) flower petal extract (CTE) is used as a natural colorant in a variety of foods and beverages. The objective of study was to determine the inhibitory effect of CTE on adipogenesis in 3T3-L1 preadipocytes. The phytochemical profiles of CTE were analyzed by liquid chromatography and tandem mass spectrometry (LC-MS/MS). Anti-adipogenesis effect of CTE was measured by using Oil Red O staining, intracellular triglyceride assay, quantitative real-time PCR and western blot analysis in 3T3-L1 adipocytes. Cell cycle studies were performed by flow cytometry. Lipolysis experiments were performed using a colorimetric assay kit. In early stages, CTE demonstrated anti-adipogenic effects through inhibition of proliferation and cell cycle retardation by suppressing expression of phospho-Akt and phospho-ERK1/2 signaling pathway. The results also showed that CTE inhibited the late stage of differentiation through diminishing expression of adipogenic transcription factors including PPARγ and C/EBPα. The inhibitory action was subsequently attenuated in downregulation of fatty acid synthase and acetyl-CoA carboxylase, causing the reduction of TG accumulation. In addition, CTE also enhanced catecholamine-induced lipolysis in adipocytes. These results suggest that CTE effectively attenuates adipogenesis by controlling cell cycle progression and downregulating adipogenic gene expression.
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Martineau, Louis, Jessica Hervé, Asim Muhamad, et al. "Anti-adipogenic Activities ofAlnus incanaandPopulus balsamiferaBark Extracts, Part I: Sites and Mechanisms of Action." Planta Medica 76, no. 13 (2010): 1439–46. http://dx.doi.org/10.1055/s-0029-1240941.
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Hyun, Jimin, Hyo-Geun Lee, Jun-Geon Je, et al. "L-Fucose-Rich Sulfated Glycans from Edible Brown Seaweed: A Promising Functional Food for Obesity and Energy Expenditure Improvement." International Journal of Molecular Sciences 25, no. 17 (2024): 9738. http://dx.doi.org/10.3390/ijms25179738.
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The global obesity epidemic, exacerbated by the sedentary lifestyle fostered by the COVID-19 pandemic, presents a growing socioeconomic burden due to decreased physical activity and increased morbidity. Current obesity treatments show promise, but they often come with expensive medications, frequent injections, and potential side effects, with limited success in improving obesity through increased energy expenditure. This study explores the potential of a refined sulfated polysaccharide (SPSL), derived from the brown seaweed Scytosiphon lomentaria (SL), as a safe and effective anti-obesity treatment by promoting energy expenditure. Chemical characterization revealed that SPSL, rich in sulfate and L-fucose content, comprises nine distinct sulfated glycan structures. In vitro analysis demonstrated potent anti-lipogenic properties in adipocytes, mediated by the downregulation of key adipogenic modulators, including 5′ adenosine monophosphate-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor γ (PPARγ) pathways. Inhibiting AMPK attenuated the anti-adipogenic effects of SPSL, confirming its involvement in the mechanism of action. Furthermore, in vivo studies using zebrafish models showed that SPSL increased energy expenditure and reduced lipid accumulation. These findings collectively highlight the therapeutic potential of SPSL as a functional food ingredient for mitigating obesity-related metabolic dysregulation by promoting energy expenditure. Further mechanistic and preclinical investigations are warranted to fully elucidate its mode of action and evaluate its efficacy in obesity management, potentially offering a novel, natural therapeutic avenue for this global health concern.
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Gagnon, AnneMarie, Charlie Foster, Anne Landry та Alexander Sorisky. "The role of interleukin 1β in the anti-adipogenic action of macrophages on human preadipocytes". Journal of Endocrinology 217, № 2 (2013): 197–206. http://dx.doi.org/10.1530/joe-12-0565.
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When adipose tissue accumulates in obesity, the ability of preadipocytes to differentiate permits a hyperplastic expansion of functional adipocytes that preserves insulin sensitivity. Adipose infiltration by macrophages is associated with an adipogenic deficit and the appearance of inflamed, insulin-resistant hypertrophied adipocytes. Interleukin 1β (IL1β) has been reported to account for the anti-adipogenic action of macrophages in a mouse model. Using the THP-1 human macrophage cell line and human primary preadipocytes, our objective was to determine whether IL1β was necessary for the ability of conditioned medium from THP-1 macrophages (THP-1-MacCM) to: i) stimulate human preadipocyte inhibitor of κB kinase β (IKKβ) and ii) inhibit human adipocyte differentiation. IL1β is present in THP-1-MacCM, and THP-1-MacCM or IL1β (500 pg/ml; its concentration in THP-1-MacCM) acutely stimulated IKKβ phosphorylation and inhibitor of κB (IκB) degradation in preadipocytes. IL1β was sufficient to inhibit adipogenesis on its own, and this was blocked by SC-514, an IKKβ inhibitor, as has been reported for THP-1-MacCM. IκB degradation by IL1β-immunodepleted THP-1-MacCM was attenuated, whereas IKKβ phosphorylation and the inhibition of adipocyte differentiation were unchanged. Therefore, in contrast to what has been suggested for mouse cell models, IL1β is not required for the ability of MacCM to inhibit adipogenesis in human cell models.
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Jakab, Jelena, Milorad Zjalić, Štefica Mikšić, et al. "Effect of Metformin and Simvastatin in Inhibiting Proadipogenic Transcription Factors." Current Issues in Molecular Biology 43, no. 3 (2021): 2082–97. http://dx.doi.org/10.3390/cimb43030144.
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Obesity is a multifactorial chronic disease characterized by the excessive accumulation of fat in adipose tissue driven by hypertrophy and hyperplasia of adipocytes through adipogenesis. Adipogenesis plays a key role in the development of obesity and related metabolic disorders, which makes it potential target for the therapeutic approach to obesity. An increasing number of studies confirm the pleiotropic action of the combined treatment with metformin and statins, suggesting their anti-hypertensive, anti-inflammatory, and anti-adipogenic effect. The aim of this study was to analyze the effect of different doses of metformin (MET) and simvastatin (SIM) on the expression of key transcription factors of adipogenesis. Mouse 3T3-L1 preadipocytes were induced to differentiation in adipogenic medium with sustained MET and SIM treatment to assess the effect on adipogenesis. Nine days after initiating adipogenesis, the cells were prepared for further experiments, including Oil Red O staining, RT-PCR, Western blotting, and immunocytochemistry. Treating the cells with the combination of MET and SIM slightly reduced the intensity of Oil Red O staining compared with the control group, and down-regulated mRNA and protein expression of PPARγ, C/EBPα, and SREBP-1C. In conclusion, the inhibitory effect of MET and SIM on adipocyte differentiation, as indicated by decreased lipid accumulation, appears to be mediated through the down-regulation of adipogenic transcription factors, peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer binding pro-tein α (C/EBPα), and sterol regulatory element-binding protein 1 (SREBP-1C).
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Krongyut, Ornnicha, and Khaetthareeya Sutthanut. "Phenolic Profile, Antioxidant Activity, and Anti-obesogenic Bioactivity of Mao Luang Fruits (Antidesma bunius L.)." Molecules 24, no. 22 (2019): 4109. http://dx.doi.org/10.3390/molecules24224109.
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To investigate the anti-obesity potential of Antidesma bunius L. (MM), a Thai local fruit which is named “Mao Luang,” we have focused on the effects on pancreatic α-amylase and lipase enzyme activity and on adipocyte life cycle using the 3T3-L1 cell line as a model. In addition, the phytochemical composition and anti-oxidation potential were also analyzed using HPLC-PDA UV and colorimetric methods. The ethanolic extract of MM fruits prepared by a maceration method was used in the experiments. MM extract, yield 12.08% w/w, is composed primarily of phenolics and anthocyanins as the major phytochemicals, among which, gallic acid, catechin, anthocyanin-3-glucoside, and protocatechuic acid were initially identified. In addition, susceptibly inhibitory effects on oxidation in a DPPH assay; on lipase enzyme activity rather than amylase enzyme; and on adipocyte adipogenesis of MM were demonstrated. Interestingly, a concentration-dependent bi-modular manner of activity on adipocyte adipogenesis was discovered, whereby a significant anti-adipogenic effect was demonstrated at high concentration, whilst low concentrations of MM showed adipogenic induction. Lipolytic induction was manifested. Conclusively, the ethanolic MM extract was discovered to be a potential anti-obesity agent contributed by inhibitory effects on lipase enzyme and anti-differentiation and -adipogenesis in adipocytes which significantly correlated to the total phenolics content, as well as anti-oxidation as the mechanism of action. Nevertheless, to achieve effective application, further investigation in in vivo models should be considered.
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Nicholson, A. C., D. P. Hajjar, X. Zhou, W. He, A. M. Gotto та J. Han. "Anti-adipogenic action of pitavastatin occurs through the coordinate regulation of PPARγ and Pref-1 expression". British Journal of Pharmacology 151, № 6 (2007): 807–15. http://dx.doi.org/10.1038/sj.bjp.0707250.
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Yang, Hee, Min Jeong Kang, Gihyun Hur та ін. "Sulforaphene Suppresses Adipocyte Differentiation via Induction of Post-Translational Degradation of CCAAT/Enhancer Binding Protein Beta (C/EBPβ)". Nutrients 12, № 3 (2020): 758. http://dx.doi.org/10.3390/nu12030758.
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Adipocyte differentiation (adipogenesis) is a crucial process that determines the total number and size of mature adipocytes that will develop. In this study, the anti-adipogenic effect of sulforaphene (SFEN), a dietary isothiocyanate (ITC) derived from radish, is investigated both in 3T3-L1 pre-adipocytes and in human adipose tissue-derived stem cells. The results revealed that SFEN significantly inhibit adipogenic cocktail-induced adipocyte differentiation and lipid accumulation at the early stage of adipogenesis. Additionally, the effects are more potent compared to those of other ITCs derived from various cruciferous vegetables. As a related molecular mechanism of action, SFEN promotes the post-translational degradation of CCAAT/enhancer-binding protein (C/EBP) β by decreasing the stability of C/EBPβ, which is responsible for decreasing the expression of master regulatory proteins such as peroxisome proliferator-activated receptor γ and C/EBPα. Collectively, these results suggest that the intake of SFEN-enriched natural materials could be helpful as a strategy for preventing obesity.
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Yu, Mi-Hee, Yun-Jeong Jeong, Sung Wook Son та ін. "Ascochlorin Attenuates the Early Stage of Adipogenesis via the Wnt/β-Catenin Pathway and Inhibits High-Fat-Diet-Induced Obesity in Mice". International Journal of Molecular Sciences 25, № 18 (2024): 10226. http://dx.doi.org/10.3390/ijms251810226.
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This study investigated the effects of ascochlorin (ASC), a natural compound derived from the fungus Ascochyta viciae, on adipogenesis and obesity. We determined the effects of ASC on 3T3-L1 preadipocytes and whether it ameliorated to mitigate high-fat diet (HFD)-induced obesity in C57BL/6J mice. We found that ASC significantly inhibited the differentiation of preadipocytes by modulating the Wnt/β-catenin signaling pathway, a key regulator of adipogenic processes. Treatment with ASC not only reduced the mRNA and protein expression of key adipogenic transcription factors such as C/EBPα and PPARγ, but also reduced lipid accumulation both in vitro and in vivo. In addition, treatment HFD-fed mice with ASC significantly reduced their weight gain and adiposity vs. control mice. These results suggest that ASC has considerable potential as a therapeutic agent for obesity, owing to its dual action of inhibiting adipocyte differentiation and reducing lipid accumulation. Thus, ASC represents a promising candidate as a natural anti-obesity agent.
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Ali, Heidari, Meftahi Gholamhosein, Bahrami Farideh, et al. "Anti-Adipogenic Effects of Eryngium billardieri Extract during 3T3-L1 Adipocyte Differentiation." Journal of Advances in Medical and Biomedical Research 31, no. 147 (2023): 391–97. https://doi.org/10.30699/jambs.31.147.391.
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<strong>Abstract:</strong> <strong>Background and Objective: </strong>Obesity is a major public health problem whose prevalence has constantly increased worldwide. Obesity is a risk factor for several diseases such as type 2 diabetes, fatty liver disease, hyperlipidemia, cardiovascular diseases, and cancer, all of which reduce the quality of life and life expectancy. This study investigated anti-adipogenic effects of <i>Eryngium billardierei</i> (Ery) extract.<strong>Materials and Methods: </strong>The nontoxic concentration of Ery extract was estimated via the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazoliu bromide (MTT) assay. The differentiation of mouse-derived 3T3-L1 preadipocytes into mature adipocytes was induced in the presence or absence of Ery extract. Then, the accumulation of lipid droplets was identified by Oil Red O staining. Triacylglycerol level and glycerol-3phosphate dehydrogenase (GPDH) activity were also measured.<strong>Results:</strong> The MTT assay showed that 3 mg/mL of the Ery extract can be a nontoxic dose for other analyses. Oil Red O staining demonstrated a reduction of lipid droplets in the extract-treated adipocyte 3T3-L1 compared to the non-treated group. A significant decrease of triacylglycerol level in the treated 3T3-L1 adipocyte (0.32±0.03 mgTG/mg protein) compared with the nontreated group (0.78±0.05 mgTG/mg protein) (P<0.01), and a significant decrease of glycerol-3-phosphate dehydrogenase (GPDH) activity in the 3T3-L1adipocyte treated (15.3±2.1 U/ml) compared to the non-treated group (30.2±3.9 U/ml) (P<0.05) confirmed the inhibitory action of Ery extract on adipocyte differentiation.<strong>Conclusion: </strong>Ery extract, as a safe herbal extract, has anti-adipogenic activity and merits more investigation as a candidate for developing an anti-obesity drug or supplement.<strong>Keywords: </strong>Adipocyte Differentiation, Eryngium billardierei, GPDH Activity, 3T3-L1 Cell Line
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Park, In Sil, Boyun Kim, Youngjin Han та ін. "Decursin and Decursinol Angelate Suppress Adipogenesis through Activation of β-catenin Signaling Pathway in Human Visceral Adipose-Derived Stem Cells". Nutrients 12, № 1 (2019): 13. http://dx.doi.org/10.3390/nu12010013.
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Visceral adiposity is closely associated with metabolic disorders and cardiovascular diseases. Angelica gigas Nakai (AGN) has been reported to possess anti-obesity effects and higher amounts of coumarin compounds are present in AGN. However, the active compounds suppressing adipogenesis in AGN and mechanisms of action have not been investigated in adipose-derived stem cells (ASCs) isolated from visceral adipose tissue (VAT). Among four coumarin compounds of AGN, decursin (D) and decursinol angelate (DA) significantly inhibited adipocyte differentiation from ASCs. D and DA downregulated CCAAT/enhancer binding protein α (C/EBPα), peroxisome proliferator-activated receptor γ (PPARγ), adipocyte fatty acid binding protein (aP2), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC) at both mRNA and protein levels. Next, treatment with adipogenic differentiation medium (ADM) on ASCs downregulated β-catenin expression at protein level, while addition of D and DA could restore protein expression and nuclear translocation of β-catenin suppressed by ADM. D and DA treatment on ADM treated ASCs increased inhibitory phosphorylation of Glycogen synthase kinase (GSK)-3β, thereby preventing β-catenin from degradation. Additionally, si-β-catenin transfection significantly upregulated protein expression of C/EBPα and PPARγ, alleviating the anti-adipogenic effect of D and DA on ADM treated ASCs. Overall, D and DA, active compounds from AGN, suppressed adipogenesis through activation of β-catenin signaling pathway in ASCs derived from human VAT, possibly using as natural anti-visceral adiposity agents.
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Vassaux, Georges, Raymond Négrel, Gérard Ailhaud, and Danielle Gaillard. "Proliferation and differentiation of rat adipose precursor cells in chemically defined medium: Differential action of anti-adipogenic agents." Journal of Cellular Physiology 161, no. 2 (1994): 249–56. http://dx.doi.org/10.1002/jcp.1041610209.
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Kwon, Hyo-Shin, and Byeong-Churl Jang. "Anti-adipogenic Effect and Mechanism in 3T3-L1 Preadipocyte Differentiation by Salvianolic Acid B." Keimyung Medical Journal 41, no. 2 (2022): 67–75. http://dx.doi.org/10.46308/kmj.2022.00213.
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Salvianolic acid B (Sal B) is one of the most active hydrophilic compounds extracted from Salvia miltiorrhiza root. Previous in vitro and in vivo studies demonstrate the ability of Sal B to modulate adipocyte differentiation. However, the lipid-modulating effect and mechanism of Sal B in adipocytes remain controversial. Here we investigated the regulatory effect and mode of action of Sal B on lipid accumulation in 3T3-L1 preadipocyte differentiation. Lipid droplet (LD) accumulation and triglyceride (TG) content during 3T3-L1 preadipocyte differentiation were measured by Oil Red O staining and AdipoRed assay. The growth inhibition during 3T3-L1 preadipocyte differentiation was measured by cell count analysis. Western blotting and real-time qPCR analysis were utilized to determine the protein and mRNA expression in the preadipocyte differentiation. Notably, in 3T3-L1 preadipocyte differentiation, treatment with Sal B at 100 M led to a marked decrease in LD accumulation and TG content without influencing cell growth. Sal B treatment (100 M) further reduced the expression and phosphorylation levels of adipogenic transcription factors, including CCAAT/enhancer-binding protein- (C/EBP-), peroxisome proliferator-activated receptor-gamma (PPAR)-, and signal transducer and activator of transcription (STAT)-3/5. Treatment with Sal B (100 M) also reduced the expression and phosphorylation levels of fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC), two lipogenic enzymes and perilipin A, an LD-binding and stabilizing protein. These results collectively demonstrate that Sal B at 100 M strongly inhibits lipid accumulation in 3T3-L1 preadipocyte differentiation, mediated through regulation of the expression and phosphorylation levels of C/EBP-, PPAR-, STAT-3/5, FAS, ACC, and perilipin.
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Aykul, Senem, Jordan Maust, Vijayalakshmi Thamilselvan, Monique Floer, and Erik Martinez-Hackert. "Smad2/3 Activation Regulates Smad1/5/8 Signaling via a Negative Feedback Loop to Inhibit 3T3-L1 Adipogenesis." International Journal of Molecular Sciences 22, no. 16 (2021): 8472. http://dx.doi.org/10.3390/ijms22168472.
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Adipose tissues (AT) expand in response to energy surplus through adipocyte hypertrophy and hyperplasia. The latter, also known as adipogenesis, is a process by which multipotent precursors differentiate to form mature adipocytes. This process is directed by developmental cues that include members of the TGF-β family. Our goal here was to elucidate, using the 3T3-L1 adipogenesis model, how TGF-β family growth factors and inhibitors regulate adipocyte development. We show that ligands of the Activin and TGF-β families, several ligand traps, and the SMAD1/5/8 signaling inhibitor LDN-193189 profoundly suppressed 3T3-L1 adipogenesis. Strikingly, anti-adipogenic traps and ligands engaged the same mechanism of action involving the simultaneous activation of SMAD2/3 and inhibition of SMAD1/5/8 signaling. This effect was rescued by the SMAD2/3 signaling inhibitor SB-431542. By contrast, although LDN-193189 also suppressed SMAD1/5/8 signaling and adipogenesis, its effect could not be rescued by SB-431542. Collectively, these findings reveal the fundamental role of SMAD1/5/8 for 3T3-L1 adipogenesis, and potentially identify a negative feedback loop that links SMAD2/3 activation with SMAD1/5/8 inhibition in adipogenic precursors.
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Karadeniz, Fatih, Jung Hwan Oh, Hyun Jin Jo та ін. "Dracunculin Inhibits Adipogenesis in Human Bone Marrow-Derived Mesenchymal Stromal Cells by Activating AMPK and Wnt/β-Catenin Signaling". International Journal of Molecular Sciences 23, № 2 (2022): 653. http://dx.doi.org/10.3390/ijms23020653.
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Increased bone marrow adiposity is widely observed in patients with obesity and osteoporosis and reported to have deleterious effects on bone formation. Dracunculin (DCC) is a coumarin isolated from Artemisia spp. but, until now, has not been studied for its bioactive potential except antitrypanosomal activity. In this context, current study has reported the anti-adipogenic effect of DCC in human bone marrow-derived mesenchymal stromal cells (hBM-MSCs). DCC dose-dependently inhibited the lipid accumulation and expression of adipogenic transcription factors peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα) in hBM-MSCs induced to undergo adipogenesis. To elucidate its action mechanism, the effect of DCC on Wnt/β-catenin and AMPK pathways was examined. Results showed that DCC treatment activated Wnt/β-catenin signaling pathway via AMPK evidenced by increased levels of AMPK phosphorylation and Wnt10b expression after DCC treatment. In addition, DCC treated adipo-induced hBM-MSCs exhibited significantly increased nuclear levels of β-catenin compared with diminished nuclear PPARγ levels. In conclusion, DCC was shown to be able to hinder adipogenesis by activating the β-catenin via AMPK, providing potential utilization of DCC as a nutraceutical against bone marrow adiposity.
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Yi, Sang Ah, Ki Hong Nam, Sil Kim, et al. "Vulpinic Acid Controls Stem Cell Fate toward Osteogenesis and Adipogenesis." Genes 11, no. 1 (2019): 18. http://dx.doi.org/10.3390/genes11010018.
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Vulpinic acid, a naturally occurring methyl ester of pulvinic acid, has been reported to exert anti-fungal, anti-cancer, and anti-oxidative effects. However, its metabolic action has not been implicated yet. Here, we show that vulpinic acid derived from a mushroom, Pulveroboletus ravenelii controls the cell fate of mesenchymal stem cells and preadipocytes by inducing the acetylation of histone H3 and α-tubulin, respectively. The treatment of 10T1/2 mesenchymal stem cells with vulpinic acid increased the expression of Wnt6, Wnt10a, and Wnt10b, which led to osteogenesis inhibiting the adipogenic lineage commitment, through the upregulation of H3 acetylation. By contrast, treatment with vulpinic acid promoted the terminal differentiation of 3T3-L1 preadipocytes into mature adipocytes. In this process, the increase in acetylated tubulin was accompanied, while acetylated H3 was not altered. As excessive generation of adipocytes occurs, the accumulation of lipid drops was not concentrated, but dispersed into a number of adipocytes. Consistently, the expressions of lipolytic genes were upregulated and inflammatory factors were downregulated in adipocytes exposed to vulpinic acid during adipogenesis. These findings reveal the multiple actions of vulpinic acid in two stages of differentiation, promoting the osteogenesis of mesenchymal stem cells and decreasing hypertrophic adipocytes, which can provide experimental evidence for the novel metabolic advantages of vulpinic acid.
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Guan, Jian, and Deok Bae Park. "Effect of Ecklonia Cava on glucose consumption in rat skeletal muscle cells." Journal of Medicine and Life Science 9, no. 1 (2012): 44–48. http://dx.doi.org/10.22730/jmls.2012.9.1.44.
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Ecklonia cava is a kind of brown sea algae and its extract has known to be anti-adipogenic, anti-inflammatory, and so on. However, It less has been known about the action mechanism in regulating glucose metabolism in skeletal muscle cells. The present study investigated the effect of the ethanol extract of Ecklonia cava (E-EC) on glucose consumption and its related signaling properties in L6 rat skeletal muscle cells. E-EC slimulated glucose consumption as well as the translocation of glucose transporter 4 (Glut4) from cytosol to plasma membrane in L6 muscle cells. E-EC also stimulated Pl3 kinase (PI3K)-dependent Akt activity, one of crucial signaling cascades for glucose uptake. Inhibition of PI3K suppresed E-EC-stimuated glucose consumption and Glut4 translocation. However, E-EC failed to stimulate AMPK. These results suggest that the extract of Ecklonia cava stimulates glucose consumption regardless insulin activity in skeletal muscle cells via PI3K- Akt pathway through stimulating Glul4 translocation to the plasma membrane.
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PARK, YU-KYOUNG, VICTOR SUKBONG HONG, TAE-YOON LEE, et al. "The novel anti-adipogenic effect and mechanisms of action of SGI-1776, a Pim-specific inhibitor, in 3T3-L1 adipocytes." International Journal of Molecular Medicine 37, no. 1 (2015): 157–64. http://dx.doi.org/10.3892/ijmm.2015.2415.
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Lee, Soo-Young, Tae-Yang Kim, Ji-Yoon Hong, et al. "Anti-Obesity and Anti-Adipogenic Effects of Administration of Arginyl-Fructose-Enriched Jeju Barley (Hordeum vulgare L.) Extract in C57BL/6 Mice and in 3T3-L1 Preadipocytes Models." Molecules 27, no. 10 (2022): 3248. http://dx.doi.org/10.3390/molecules27103248.
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In our previous study, we reported that arginyl-fructose (AF), one of the Amadori rearrangement compounds (ARCs) produced by the heat processing of Korean ginseng can reduce carbohydrate absorption by inhibiting intestinal carbohydrate hydrolyzing enzymes in both in vitro and in vivo animal models. This reduced absorption of carbohydrate might be helpful to control body weight gain due to excessive carbohydrate consumption and support induced calorie restriction. However, the weight management effect, except for the effect due to anti-hyperglycemic action, along with the potential mechanism of action have not yet been determined. Therefore, the efforts of this study are to investigate and understand the possible weight management effect and mechanism action of AF-enriched barley extracts (BEE). More specifically, the effect of BEE on lipid accumulation and adipogenic gene expression, body weight gain, body weight, plasma lipids, body fat mass, and lipid deposition were evaluated using C57BL/6 mice and 3T3-L1 preadipocytes models. The formation of lipid droplets in the 3T3-L1 treated with BEE (500 and 750 µg/mL) was significantly blocked (p < 0.05 and p < 0.01, respectively). Male C57BL/6 mice were fed a high-fat diet (30% fat) for 8 weeks with BEE (0.3 g/kg-body weight). Compared to the high fat diet control (HFD) group, the cells treated with BEE significantly decreased in intracellular lipid accumulation with concomitant decreases in the expression of key transcription factors, peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein alpha (CEBP/α), the mRNA expression of downstream lipogenic target genes such as fatty acid binding protein 4 (FABP4), fatty acid synthase (FAS), and sterol regulatory element-binding protein 1c (SREBP-1c). Supplementation of BEE effectively lowered the body weight gain, visceral fat accumulation, and plasma lipid concentrations. Compared to the HFD group, BEE significantly suppressed body weight gain (16.06 ± 2.44 g vs. 9.40 ± 1.39 g, p < 0.01) and increased serum adiponectin levels, significantly, 1.6-folder higher than the control group. These results indicate that AF-enriched barley extracts may prevent diet-induced weight gain and the anti-obesity effect is mediated in part by inhibiting adipogenesis and increasing adiponectin level.
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Cheng, Hsin-Lin, Wei-Tang Chang, Jiun-Ling Lin, et al. "An Innovative Mei-Gin Formula Exerts Anti-Adipogenic and Anti-Obesity Effects in 3T3-L1 Adipocyte and High-Fat Diet-Induced Obese Rats." Foods 12, no. 5 (2023): 945. http://dx.doi.org/10.3390/foods12050945.
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Background: To investigate the potential anti-obesity properties of an innovative functional formula (called the Mei-Gin formula: MGF) consisting of bainiku-ekisu, Prunus mume (70% ethanol extract), black garlic (water extract), and Mesona procumbens Hemsl. (40% ethanol extract) for reducing lipid accumulation in 3T3-L1 adipocytes in vitro and obese rats in vivo. Material and Methods: The prevention and regression of high-fat diet (HFD)-induced obesity by the intervention of Japan Mei-Gin, MGF-3 and -7, and positive health supplement powder were investigated in male Wistar rats. The anti-obesity effects of MGF-3 and -7 in rats with HFD-induced obesity were examined by analyzing the role of visceral and subcutaneous adipose tissue in the development of obesity. Results: The results indicated that MGF-1-7 significantly suppressed lipid accumulation and cell differentiation through the down-regulation of GPDH activity, as a key regulator in the synthesis of triglycerides. Additionally, MGF-3 and MGF-7 exhibited a greater inhibitory effect on adipogenesis in 3T3-L1 adipocytes. The high-fat diet increased body weight, liver weight, and total body fat (visceral and subcutaneous fat) in obese rats, while these alterations were effectively improved by the administration of MGF-3 and -7, especially MGF-7. Conclusion: This study highlights the role of the Mei-Gin formula, particularly MGF-7, in anti-obesity action, which has the potential to be used as a therapeutic agent for the prevention or treatment of obesity.
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Li, L., L. Tam, L. Liu, T. Jin, and D. S. Ng. "Wnt-signaling mediates the anti-adipogenic action of lysophosphatidic acid through cross talking with the Rho/Rho associated kinase (ROCK) pathway." Biochemistry and Cell Biology 89, no. 6 (2011): 515–21. http://dx.doi.org/10.1139/o11-048.
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Lysophosphatidic acid (LPA) is a bioactive phospholipid with a diverse range of biological activities including the modulation of adipogenesis. Treatment of 3T3-L1 cells and 3T3F44A cells with LPA inhibits adipogenesis and reduces expression of PPARγ through activation of RhoGTPase and its downstream Rho associated kinase (ROCK). The mechanism of suppression of PPARγ expression by Rho/ROCK is poorly understood. By treating the differentiating 3T3-L1 cells with various combinations of LPA and ROCK inhibitors, Y-27632 and fasudil, we observed that LPA treatment resulted in attenuation of adipogenesis and a significant reduction in PPARγ mRNA as early as 3 d post-induction. LPA treatment also resulted in significant but delayed upregulation of components of the canonical Wnt signaling, namely Wnt10b mRNA, β-catenin protein, and mRNA expression of β-catenin target genes, detectable at day 7, but not day 3. Treatment of the 3T3-L1 cells with ROCK inhibitors Y-27632 and fasudil revealed a tonic activation of β-catenin/target genes by ROCK. This study identified the existence of a novel cross talk between the Rho/ROCK pathway and the Wnt-signaling pathway. The LPA/Rho/ROCK pathway inhibits expression of PPARγ and adipogenesis in part through a delayed activation of the canonical Wnt-signaling pathway based on increased Wnt10b expression and β-catenin induction.
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Chao, Pei-Min, Hui-Ling Huang, Chun-Huei Liao, Shiau-Ting Huang, and Ching-jang Huang. "A high oxidised frying oil content diet is less adipogenic, but induces glucose intolerance in rodents." British Journal of Nutrition 98, no. 1 (2007): 63–71. http://dx.doi.org/10.1017/s000711450769000x.
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Oxidised frying oil (OFO) and fish oil have been shown to be peroxisome proliferator-activated receptor (PPAR)α activators and their ingestion results in pleotropic peroxisome proliferator responses in rats. To examine the effect of dietary OFO on adiposity, four groups of weanling Sprague–Dawley rats were fed isoenergetically with, respectively, a low fat basal diet containing 5 g/100 g of fresh soybean oil (LSB) or a high fat diet containing 20 g/100 g of fresh soybean oil (HSB), OFO (HO) or fish oil (HF). The tissue mass, cell size and lipid/DNA ratio in the retroperitoneal fat pad and serum leptin levels were lowest in the HO group (P < 0·05), indicating that dietary OFO has a greater anti-adipogenic action than dietary fish oil. However, a tendency to hyperglycaemia was observed in the HO group (P = 0·0528). To examine the effect of dietary OFO on glucose tolerance, three groups of rats and three groups of mice were fed, respectively, the LSB, HSB or HO diet, and an oral glucose tolerance test was performed. After oral glucose load, the area under the curve for blood glucose (AUCglu) over 2 h was significantly higher, and that for serum insulin (AUCins) over 90 min was significantly lower, in the HO group than in the other two groups (P < 0·05). These results demonstrate that, in rats and mice, a high OFO diet is less adipogenic, but induces glucose intolerance.
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Yadav, Anil Kumar, and Byeong-Churl Jang. "Inhibition of Lipid Accumulation and Cyclooxygenase-2 Expression in Differentiating 3T3-L1 Preadipocytes by Pazopanib, a Multikinase Inhibitor." International Journal of Molecular Sciences 22, no. 9 (2021): 4884. http://dx.doi.org/10.3390/ijms22094884.
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Pazopanib is a multikinase inhibitor with anti-tumor activity. As of now, the anti-obesity effect and mode of action of pazopanib are unknown. In this study, we investigated the effects of pazopanib on lipid accumulation, lipolysis, and expression of inflammatory cyclooxygenase (COX)-2 in differentiating and differentiated 3T3-L1 cells, a murine preadipocyte. Of note, pazopanib at 10 µM markedly decreased lipid accumulation and triglyceride (TG) content during 3T3-L1 preadipocyte differentiation with no cytotoxicity. Furthermore, pazopanib inhibited not only expression of CCAAT/enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), and perilipin A but also phosphorylation of signal transducer and activator of transcription (STAT)-3 during 3T3-L1 preadipocyte differentiation. In addition, pazopanib treatment increased phosphorylation of cAMP-activated protein kinase (AMPK) and its downstream effector ACC during 3T3-L1 preadipocyte differentiation. However, in differentiated 3T3-L1 adipocytes, pazopanib treatment did not stimulate glycerol release and hormone-sensitive lipase (HSL) phosphorylation, hallmarks of lipolysis. Moreover, pazopanib could inhibit tumor necrosis factor (TNF)-α-induced expression of COX-2 in both 3T3-L1 preadipocytes and differentiated cells. In summary, this is the first report that pazopanib has strong anti-adipogenic and anti-inflammatory effects in 3T3-L1 cells, which are mediated through regulation of the expression and phosphorylation of C/EBP-α, PPAR-γ, STAT-3, ACC, perilipin A, AMPK, and COX-2.
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Savova, Martina, Monika Todorova, Apostol Apostolov, Galina Yahubyan, and Milen Georgiev. "Betulinic acid counteracts the lipid accumulation in Caenorhabditis elegans by modulation of nhr-49 expression." Biomedicine & Pharmacotherapy 156 (October 12, 2022): 113862. https://doi.org/10.1016/j.biopha.2022.113862.
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Obesity is an ingrained health problem with а multifactorial origin and а long history, thereby innovations in the treatment strategies are of great importance. In the search of a remedy for excessive weight gain, we have directed our investigations to phytochemicals as valuable bioactive compounds. Betulinic acid (BA), among the other triterpenoids, is known for its anti-inflammatory and anti-neoplastic properties. In addition, a previous study of ours has demonstrated а potent anti-adipogenic effect of BA in human adipocytes. Therefore, we aimed here to further verify the anti-obesogenic effect of BA in vivo in Caenorhabditis elegans. Induction of lipid accumulation in the nematodes was modelled with glucose-supplemented media, followed by treatment with BA (10–50 μM) or orlistat (12 μM) as a control anti-obesity medication. Oil red O and Nile red staining were applied to provide quantification of accumulated lipids. Analysis of the relative expression of genes, related to lipid metabolism suggested molecular mechanism of lipid-reducing action of BA in C. elegans. Treatment of nematodes with BA significantly decreased the lipid accumulation, downregulated desaturases involved in lipogenesis (fat-5, fat-6 and fat-7), modulated key transcription factors (nhr-49 and hlh-11) and microRNAs (miR-60, lin-4, let-7 and miR-786) associated with the lipid metabolism. Collectively, the current research provides additional insight on the molecular mechanism of the BA’s anti-obesogenic effect in vivo. Furthermore, it validates the potential of BA as a candidate compound in obesity management by reducing lipid accumulation.
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Lee, Eunyoung, Emily L. Miedzybrodzka, Xilin Zhang, et al. "Diet-Induced Obese Mice and Leptin-Deficient Lepob/ob Mice Exhibit Increased Circulating GIP Levels Produced by Different Mechanisms." International Journal of Molecular Sciences 20, no. 18 (2019): 4448. http://dx.doi.org/10.3390/ijms20184448.
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As glucose-dependent insulinotropic polypeptide (GIP) possesses pro-adipogenic action, the suppression of the GIP hypersecretion seen in obesity might represent a novel therapeutic approach to the treatment of obesity. However, the mechanism of GIP hypersecretion remains largely unknown. In the present study, we investigated GIP secretion in two mouse models of obesity: High-fat diet-induced obese (DIO) mice and leptin-deficient Lepob/ob mice. In DIO mice, plasma GIP was increased along with an increase in GIP mRNA expression in the lower small intestine. Despite the robust alteration in the gut microbiome in DIO mice, co-administration of maltose and the α-glucosidase inhibitor (α-GI) miglitol induced the microbiome-mediated suppression of GIP secretion. The plasma GIP levels of Lepob/ob mice were also elevated and were suppressed by fat transplantation. The GIP mRNA expression in fat tissue was not increased in Lepob/ob mice, while the expression of an interleukin-1 receptor antagonist (IL-1Ra) was increased. Fat transplantation suppressed the expression of IL-1Ra. The plasma IL-1Ra levels were positively correlated with the plasma GIP levels. Accordingly, although circulating GIP levels are increased in both DIO and Lepob/ob mice, the underlying mechanisms differ, and the anti-obesity actions of α-GIs and leptin sensitizers may be mediated partly by the suppression of GIP secretion.
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Jin, Bo-Ram, Kyung-Sook Chung, Minho Lee, and Hyo-Jin An. "High-Fat Diet Propelled AOM/DSS-Induced Colitis-Associated Colon Cancer Alleviated by Administration of Aster glehni via STAT3 Signaling Pathway." Biology 9, no. 2 (2020): 24. http://dx.doi.org/10.3390/biology9020024.
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Many epidemiological observational studies suggest that a high-fat diet (HFD) accelerates the risk of colorectal cancer (CRC). Inflammation can play a key role in the relationship between colon cancer and HFD. Although reported by several studies, controlled experimental studies have not explored this relationship. We established an HFD-fed colitis-associated colon cancer (CAC) mice model and evaluated the anti-tumorigenic effects of AG on HFD-propelled CAC along with its mechanism of action. Previously, we found that Aster glehni (AG) exerts chemopreventive effects on azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced CAC in a mice model, and has anti-adipogenic effects in a HFD-induced obesity mice model. In the HFD-propelled CAC mice model, AG significantly reduced cancer-related death, prevented body weight loss, and alleviated splenic enlargement. Additionally, AG prevented colon shortening and reduced the number of colorectal polyps. Histological studies demonstrated the up-regulation of inflammation, hyperplasia, and neoplasia in HFD-propelled CAC mice, whereas AG suppressed colonic disease progression and tumorigenesis. Furthermore, AG significantly inhibited the signal transducer and activator of transcription 3 (STAT3) signaling pathway and attenuated the protein expression of the STAT3 target gene, which mediates transcription factor-dependent tumor cell proliferation. These results indicate that AG abrogates inflammation-induced tumor progression in HFD-propelled CAC mice by inhibiting STAT3 activation.
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Yadav, Rita, Munesh Mani, and Ramandeep Kaur. "A COMPREHENSIVE REVIEW ON ANTI-OBESITY POTENTIAL OF CYPERUS ROTUNDUS IN EXPERIMENTAL ANIMALS." YMER Digital 21, no. 07 (2022): 144–53. http://dx.doi.org/10.37896/ymer21.07/11.
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Worldwide, obesity and the illnesses it causes have become serious health issues, and obesity is today the fifth most common cause of death. According to research, there were 641 million obese adults worldwide in 2014. This review was based on detailing of obesity, BMI ranges, anti-obesity potential and signalling pathways of Cyperus rotundus. It covered extensive literature survey from the studies published in PubMed, Elsevier, Google Scholar etc. A member of the Cyperaceae family, Cyperus rotundus grows naturally in tropical and temperate climates and has long been used to heal mental and digestive issues. In order to determine the effectiveness and safety of Cyperus rotundus rhizome extract (CRE), which is standardised to contain Piceatannol, Scirpusin A, and Scirpusin B (5 percent total Stilbenoids), in overweight people, studies have been conducted. Cyperus rotundus has shown dietary enzyme inhibitory action when observed. It significantly lowered the level of all three enzymes i.e., Lipase, Alphaamylase and Alpha- glucosidase. Changes in cell shape and the concentrations of cytoskeletal and extracellular components signal the beginning of adipogenesis. As a result of this process, CCAAT-enhancerbinding proteins (C/EBP) and peroxisome proliferator-activated receptors (PPAR) that are predicated on adipogenicity begin to express themselves. In overweight people, the extract proved successful in lowering body weight and BMI. CRE might prevent obese mice from gaining weight and demonstrated anti-adipogenic effect in differentiated 3T3 L1 adipocytes in-vitro. In conclusion, many current studies have proved for its anti-obesity and lipid lowering potential in various animal or human models. It would be great change towards human use if it is developed into any suitable dosage form for better bioavailability. Keywords: Cyperus rotundus, anti-obesity, anti-hyperlipidaemic, rats, human
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Thalia, Odile Patrick, and Bizimana Rukundo T. "Plant-Derived Flavonoids as Natural Inhibitors of Adipogenesis and Glucose Dysregulation in Obese Diabetic Patients." RESEARCH INVENTION JOURNAL OF SCIENTIFIC AND EXPERIMENTAL SCIENCES 5, no. 2 (2025): 36–41. https://doi.org/10.59298/rijses/2025/52364.
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The escalating global prevalence of obesity and type 2 diabetes mellitus (T2DM) necessitates innovative therapeutic approaches to address the intertwined pathologies of adipogenesis and glucose dysregulation. Flavonoids, a heterogeneous group of polyphenolic compounds ubiquitously present in plant-based foods, have emerged as dual-action agents capable of suppressing adipose tissue expansion and enhancing glycemic control. This review consolidates contemporary research on the molecular mechanisms underpinning the anti-adipogenic and glucose-lowering effects of flavonoids, including their modulation of key pathways such as PPARγ, Wnt/β-catenin, AMPK, and PI3K/Akt. Preclinical studies underscore their efficacy in reducing adipocyte differentiation and improving insulin sensitivity, while clinical trials reveal mixed outcomes attributed to bioavailability limitations and interindividual variability. We explore therapeutic strategies to optimize flavonoid bioavailability, such as nanoformulations and dietary synergies, and propose future research directions, including personalized nutrition and combination therapies with conventional antidiabetic agents. By bridging preclinical insights with translational challenges, this review highlights flavonoids as promising candidates for holistic management of metabolic disorders, advocating for rigorous clinical validation to harness their full therapeutic potential. Keywords: Flavonoids, Adipogenesis, Glucose Metabolism, Obesity, Diabetes, Insulin Resistance, Metabolic Syndrome, Natural Products, Therapeutic Applications
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Thalia, Odile Patrick, and Bizimana Rukundo T. "Plant-Derived Flavonoids as Natural Inhibitors of Adipogenesis and Glucose Dysregulation in Obese Diabetic Patients." RESEARCH INVENTION JOURNAL OF SCIENTIFIC AND EXPERIMENTAL SCIENCES 5, no. 2 (2025): 36–41. https://doi.org/10.59298/rijses/2025/523641.
Full textAbstract:
The escalating global prevalence of obesity and type 2 diabetes mellitus (T2DM) necessitates innovative therapeutic approaches to address the intertwined pathologies of adipogenesis and glucose dysregulation. Flavonoids, a heterogeneous group of polyphenolic compounds ubiquitously present in plant-based foods, have emerged as dual-action agents capable of suppressing adipose tissue expansion and enhancing glycemic control. This review consolidates contemporary research on the molecular mechanisms underpinning the anti-adipogenic and glucose-lowering effects of flavonoids, including their modulation of key pathways such as PPARγ, Wnt/β-catenin, AMPK, and PI3K/Akt. Preclinical studies underscore their efficacy in reducing adipocyte differentiation and improving insulin sensitivity, while clinical trials reveal mixed outcomes attributed to bioavailability limitations and interindividual variability. We explore therapeutic strategies to optimize flavonoid bioavailability, such as nanoformulations and dietary synergies, and propose future research directions, including personalized nutrition and combination therapies with conventional antidiabetic agents. By bridging preclinical insights with translational challenges, this review highlights flavonoids as promising candidates for holistic management of metabolic disorders, advocating for rigorous clinical validation to harness their full therapeutic potential. Keywords: Flavonoids, Adipogenesis, Glucose Metabolism, Obesity, Diabetes, Insulin Resistance, Metabolic Syndrome, Natural Products, Therapeutic Applications.
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Silvestro, Serena, Luigi Chiricosta, Agnese Gugliandolo, et al. "Extracellular Vesicles Derived from Human Gingival Mesenchymal Stem Cells: A Transcriptomic Analysis." Genes 11, no. 2 (2020): 118. http://dx.doi.org/10.3390/genes11020118.
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Human gingival mesenchymal stem cells (hGMSCs) have outstanding characteristics of proliferation and are able to differentiate into osteogenic, chondrogenic, adipogenic, and neurogenic cell lineages. The extracellular vesicles (EVs) secreted by hGMSCs contain proteins, lipids, mRNA and microRNA have emerged as important mediators of cell-to-cell communication. In this study, we analyzed the transcriptome of hGMSCs-derived EVs using Next Generation Sequencing (NGS). The functional evaluation of the transcriptome highlighted 26 structural protein classes and the presence of “non-coding RNAs”. Our results showed that EVs contain several growth factors such as Transforming Growth Factor-β (TGF-β), Fibroblast Growth Factor (FGF), and Vascular Endothelial Growth Factors (VEGF) implicated in osteoblast differentiation and in angiogenetic process. Furthermore, the transcriptomic analysis showed the presence of glial cell-derived neurotrophic factor (GDNF) family ligands and neurotrophins involved in neuronal development. The NGS analysis also identified the presence of several interleukins among which some with anti-inflammatory action. Moreover, the transcriptome profile of EVs contained members of the Wnt family, involved in several biological processes, such as cellular proliferation and tissue regeneration. In conclusion, the huge amount of growth factors included in the hGMSCs-derived EVs could make them a big resource in regenerative medicine.
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Grigorova, Natalia, Zhenya Ivanova, Ekaterina Vachkova, Valeria Petrova, and Toncho Penev. "DHA-Provoked Reduction in Adipogenesis and Glucose Uptake Could Be Mediated by Gps2 Upregulation in Immature 3T3-L1 Cells." International Journal of Molecular Sciences 24, no. 17 (2023): 13325. http://dx.doi.org/10.3390/ijms241713325.
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The signaling pathway of fatty acids in the context of obesity is an extensively explored topic, yet their primary mechanism of action remains incompletely understood. This study aims to examine the effect of docosahexaenoic acid (DHA) on some crucial aspects of adipogenesis in differentiating 3T3-L1 cells, using palmitic acid-treated (PA), standard differentiated, and undifferentiated adipocytes as controls. Employing 60 µM DHA or PA, 3T3-L1 preadipocytes were treated from the onset of adipogenesis, with negative and positive controls included. After eight days, we performed microscopic observations, cell viability assays, the determination of adiponectin concentration, intracellular lipid accumulation, and gene expression analysis. Our findings demonstrated that DHA inhibits adipogenesis, lipolysis, and glucose uptake by suppressing peroxisome proliferator-activated receptor gamma (Pparg) and G-protein coupled receptor 120 (Gpr120) gene expression. Cell cytotoxicity was ruled out as a causative factor, and β-oxidation involvement was suspected. These results challenge the conventional belief that omega-3 fatty acids, acting as Pparg and Gpr120 agonists, promote adipogenesis and enhance insulin-dependent glucose cell flux. Moreover, we propose a novel hypothesis suggesting the key role of the co-repressor G protein pathway suppressor 2 in mediating this process. Additional investigations are required to elucidate the molecular mechanisms driving DHA’s anti-adipogenic effect and its broader health implications.
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Mukherjee, Siddhartha, Noopur Raje, Chirayu Patel, et al. "Bortezomib Induces Proliferation of Mesenchymal Progenitor Cells and Promotes Differentiation towards Osteoblastic Lineage." Blood 108, no. 11 (2006): 88. http://dx.doi.org/10.1182/blood.v108.11.88.88.
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Abstract Bortezomib is a first-in-class proteasome inhibitor approved for the therapy of relapsed, refractory multiple myeloma (MM). Two large registration trials (SUMMIT and APEX) of bortezomib in MM revealed an increase in the serum levels of bone-specific alkaline phosphatase (b-ALP) and osteocalcin (ocn) in bortezomib-responsive patients, raising the prospect that bortezomib may influence the bone marrow (BM) microenvironment in association with its anti-myeloma effect,. However, the precise cellular target of bortezomib within the BM milieu remains unknown. We hypothesized that the observed rise in b-ALP and ocn was the result of direct effects of bortezomib on osteoblast-lineage committed cells. The effect of bortezomib on osteoblastic cells was first evaluated in in vitro. When bortezomib was added to freshly isolated primary BM mononuclear cells, the CFU-Ob (osteoblastic colony-forming units) was unchanged, but the colony size was increased, with a maximum effect observed at 1 nM. In particular, bortezomib increased the number of CD45−/CD51+ cells 1.8 fold (P&lt;0.05), while no change was noted in the CD45+ (hematopoietic) cells. These CD45−/CD51+ cells expressed Collagen-1 and b-ALP, rapidly formed VanKossa+ bone nodules in vitro and lacked the expression of Sca1 and Collagen-II, suggesting that they were of osteoblastic lineage. When mice were treated with bortezomib (0.1mg/kg biw for 3 weeks), a significant increase in CD45−/CD51+ cells was observed in the bone marrow suggesting bortezomib increases the number of osteoblast-lineage cells in vivo. Next, we sought to identify the target cell for bortezomib activity. We treated CD45− BMSCs with bortezomib in vitro for 7 days and then exposed these cells to either adipogenic or osteogenic media (with bortezomib now removed). Interestingly, both differentiated osteoblasts (i.e Van-Kossa+ cells) and adipocytes (Oil-Red staining cells) were increased, suggesting that bortezomib increases the proliferation of a bipotent MPC. We then studied the impact of bortezomib on the commitment of MPCs towards osteoblastic or adipocytic lineages by culturing CD45− cells in osteogenic and adipogenic media with concurrent treatment with bortezomib. In these conditions, we found an increased number of Alk-Phos + osteoblasts in bortezomib-treated cells and a decreased number of adipocytes in adipogenic media. These data suggest that bortezomib (a) increases the proliferation of uncommitted MPCs and (b) promotes the differentiation towards osteoblastic lineage. To investigate the mechanism of bortezomib action, we studied the effect of forskolin, a cyclic AMP analogue known to accelerate the ubiquitin-mediated degradation of RUNX-2, the master-regulator of osteogenic differentiation. Forskolin treatment abrogated the effect of bortezomib on CD45− BMSCs, suggesting that bortezomib activity is influenced by the adenylate cyclase pathway, possibly through bortezomib-mediated inhibition of RUNX-2 degradation. Bortezomib alters primitive mesenchymal cell function causing increased osteoblast lineage cells.
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Lacasa, Danièle, Soraya Taleb, Mayoura Keophiphath, Alexandra Miranville, and Karine Clement. "Macrophage-Secreted Factors Impair Human Adipogenesis: Involvement of Proinflammatory State in Preadipocytes." Endocrinology 148, no. 2 (2007): 868–77. http://dx.doi.org/10.1210/en.2006-0687.
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Obesity is considered a chronic low-grade inflammatory state. The white adipose tissue produces a variety of inflammation-related proteins whose expression is increased in obese subjects. The nonadipose cell fraction, which includes infiltrated macrophages, is a determinant source of inflammation-related molecules within the adipose tissue. Our working hypothesis is that macrophage infiltration affects fat expansion through a paracrine action on adipocyte differentiation. Human primary preadipocytes were then differentiated in the presence of conditioned media obtained from macrophages differentiated from blood monocytes. Preadipocytes treated by macrophage-conditioned medium displayed marked reduction of adipogenesis as assessed by decreased cellular lipid accumulation and reduced gene expression of adipogenic and lipogenic markers. In addition to this effect, the activation of macrophages by lipopolysaccharides stimulated nuclear factor κB signaling, increased gene expression and release of proinflammatory cytokines and chemokines, and induced preadipocyte proliferation. This phenomenon was associated with increased cyclin D1 gene expression and maintenance of the fibronectin-rich matrix. Anti-TNFα neutralizing antibody inhibits the inflammatory state of preadipocytes positioning TNFα as an important mediator of inflammation in preadipocytes. Strikingly, conditioned media produced by macrophages isolated from human adipose tissue exerted comparable effects with activated macrophages, i.e. decreased adipogenesis and increased inflammatory state in the preadipocytes. These data show that macrophage-secreted factors inhibit the formation of mature adipocytes, suggesting possible role in limiting adipose tissue expansion in humans.
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Park, Jae-Eun, та Ji-Sook Han. "(E)-5-hydroxy-7-methoxy-3-(2-hydroxybenzyl)-4-chromanone, a Major Homoisoflavonoid, Attenuates Free Fatty Acid-Induced Hepatic Steatosis by Activating AMPK and PPARα Pathways in HepG2 Cells". Nutrients 16, № 20 (2024): 3475. http://dx.doi.org/10.3390/nu16203475.
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Background: (E)-5-hydroxy-7-methoxy-3-(2-hydroxybenzyl)-4-chromanone (HMC), a homoisoflavonoid isolated from Portulaca oleracea, has significant anti-adipogenesis potential; it regulates adipogenic transcription factors. However, whether HMC improves hepatic steatosis in hepatocytes remains vague. This study investigated whether HMC ameliorates hepatic steatosis in free fatty acid-treated human hepatocellular carcinoma (HepG2) cells, and if so, its mechanism of action was analyzed. Methods: Hepatic steatosis was induced by a free fatty acid mixture in HepG2 cells. Thereafter, different HMC concentrations (10, 30, and 50 µM) or fenofibrate (10 µM, a PPARα agonist, positive control) was treated in HepG2 cells.Results: HMC markedly decreased lipid accumulation and triglyceride content in free fatty acid-treated HepG2 cell; it (10 and 50 μM) markedly upregulated protein expressions of pAMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase. HMC (10 and 50 μM) markedly inhibited the expression of sterol regulatory element-binding protein-1c, fatty acid synthase, and stearoyl-coA desaturase 1, which are the enzymes involved in lipid synthesis. Furthermore, HMC (10 and 50 μM) markedly upregulated the protein expression of peroxisome proliferator-activated receptor alpha (PPARα) and enhanced the protein expressions of carnitine palmitoyl transferase 1 and acyl-CoA oxidase 1. Conclusion: HMC inhibits lipid accumulation and promotes fatty acid oxidation by AMPK and PPARα pathways in free fatty acid-treated HepG2 cells, thereby attenuating hepatic steatosis.
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Lutzow, Ylva Strandberg, Christian Gray та Ross Tellam. "15-Deoxy-Δ12,14-prostaglandin J2 induces chemokine expression, oxidative stress and microfilament reorganization in bovine mammary epithelial cells". Journal of Dairy Research 75, № 1 (2008): 55–63. http://dx.doi.org/10.1017/s0022029907003056.
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The roles of the pro-adipogenic ligands of the transcription factor Peroxisome Proliferator Activated Receptor gamma (PPARG) in regulating innate immune responses in bovine mammary epithelial cells (bMEC) were investigated using quantitative real-time PCR. The analyses revealed that 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) enhanced the expression of Interleukin 8 (IL-8) and Chemokine (C-X-C motif) ligand 6 (CXCL6) in these cells in a dose-dependent manner. 15d-PGJ2 also induced the expression of transcripts encoding proteins involved in oxidative stress, including Ferritin heavy chain and Superoxide dismutase 1, as well as substantial microfilament reorganization. In contrast, synthetic PPARG agonists displayed a different and much smaller range of effects on the cells, causing down-regulation of Interleukin 1-beta, Interleukin 6 and IL-8 and increased expression of Chemokine (C-C motif) ligand 2 (CCL2) and Tumour necrosis factor alpha (TNFα). In an independent analysis, the cells were pre-incubated with PPARG agonists followed by lipopolysaccharide stimulation. This study revealed that troglitazone increased the responsiveness of the cells to lipopolysaccharide resulting in up-regulation of Interleukin 1-beta, TNFα, IL-8, CCL2 and CXCL6 while 15d-PGJ2 caused down-regulation of TNFα, CCL2 and CXCL6. These findings are relevant to understanding the anti-inflammatory potential of the PPARG ligands and underline different mechanisms of action of 15d-PGJ2 and troglitazone in bMEC. Furthermore, the present results demonstrate that the generation of pro-inflammatory mediators can be modulated by currently available therapeutic agents and may therefore be of value in the treatment of mastitis in ruminants.
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Silvestri, Elena, Rosalba Senese, Federica Cioffi, et al. "3,5-Diiodo-L-Thyronine Exerts Metabolically Favorable Effects on Visceral Adipose Tissue of Rats Receiving a High-Fat Diet." Nutrients 11, no. 2 (2019): 278. http://dx.doi.org/10.3390/nu11020278.
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When administered to rats receiving a high-fat diet (HFD), 3,5-diiodo-L-thyronine (3,5-T2) [at a dose of 25 μg/100 g body weight (BW)] is known to increase energy expenditure and to prevent HFD-induced adiposity. Here, we investigated which cellular and molecular processes in visceral white adipose tissue (VAT) contributed to the beneficial effect of 3,5-T2 over time (between 1 day and 4 weeks following administration). 3,5-T2 programmed the adipocyte for lipolysis by rapidly inducing hormone sensitive lipase (HSL) phosphorylation at the protein kinase A-responsive site Ser563, accompanied with glycerol release at the 1-week time-point, contributing to the partial normalization of adipocyte volume with respect to control (N) animals. After two weeks, when the adipocyte volumes of HFD-3,5-T2 rats were completely normalized to those of the controls (N), 3,5-T2 consistently induced HSL phosphorylation at Ser563, indicative of a combined effect of 3,5-T2-induced adipose lipolysis and increasing non-adipose oxidative metabolism. VAT proteome analysis after 4 weeks of treatment revealed that 3,5-T2 significantly altered the proteomic profile of HFD rats and produced a marked pro-angiogenic action. This was associated with a reduced representation of proteins involved in lipid storage or related to response to oxidative stress, and a normalization of the levels of those involved in lipogenesis-associated mitochondrial function. In conclusion, the prevention of VAT mass-gain by 3,5-T2 occurred through different molecular pathways that, together with the previously reported stimulation of resting metabolism and liver fatty acid oxidation, are associated with an anti adipogenic/lipogenic potential and positively impact on tissue health.
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Quarta, Stefano, Egeria Scoditti, Maria Annunziata Carluccio та ін. "Coffee Bioactive N-Methylpyridinium Attenuates Tumor Necrosis Factor (TNF)-α-Mediated Insulin Resistance and Inflammation in Human Adipocytes". Biomolecules 11, № 10 (2021): 1545. http://dx.doi.org/10.3390/biom11101545.
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Although coffee consumption has been historically associated with negative health outcomes, recent evidence suggests a lower risk of metabolic syndrome, obesity and diabetes among regular coffee drinkers. Among the plethora of minor organic compounds assessed as potential mediators of coffee health benefits, trigonelline and its pyrolysis product N-methylpyridinium (NMP) were preliminary shown to promote glucose uptake and exert anti-adipogenic properties. Against this background, we aimed at characterizing the effects of trigonelline and NMP in inflamed and dysfunctional human adipocytes. Human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes were treated with NMP or, for comparison, trigonelline, for 5 h before stimulation with tumor necrosis factor (TNF)-α. NMP at concentrations as low as 1 µmol/L reduced the stimulated expression of several pro-inflammatory mediators, including C-C Motif chemokine ligand (CCL)-2, C-X-C Motif chemokine ligand (CXCL)-10, and intercellular adhesion Molecule (ICAM)-1, but left the induction of prostaglandin G/H synthase (PTGS)2, interleukin (IL)-1β, and colony stimulating factor (CSF)1 unaffected. Furthermore, NMP restored the downregulated expression of adiponectin (ADIPOQ). These effects were functionally associated with downregulation of the adhesion of monocytes to inflamed adipocytes. Under the same conditions, NMP also reversed the TNF-α-mediated suppression of insulin-stimulated Ser473 Akt phosphorylation and attenuated the induction of TNF-α-stimulated lipolysis restoring cell fat content. In an attempt to preliminarily explore the underlying mechanisms of its action, we show that NMP restores the expression of the master regulator of adipocyte differentiation peroxisome proliferator-activated receptor (PPAR)γ and downregulates activation of the pro-inflammatory mitogen-activated protein jun N-terminal kinase (JNK). In conclusion, NMP reduces adipose dysfunction in pro-inflammatory activated adipocytes. These data suggest that bioactive NMP in coffee may improve the inflammatory and dysmetabolic milieu associated with obesity.