scholarly journals Antiadipogenic Effects of Mixtures of Cornus officinalis and Ribes fasciculatum Extracts on 3T3-L1 Preadipocytes and High-Fat Diet-Induced Mice

Molecules ◽  
2020 ◽  
Vol 25 (10) ◽  
pp. 2350 ◽  
Author(s):  
Eunkuk Park ◽  
Chang Gun Lee ◽  
Hyesoo Jeong ◽  
Subin Yeo ◽  
Ji Ae Kim ◽  
...  
Keyword(s):  
Medicinal Plants ◽  
High Fat Diet ◽  
Adipocyte Differentiation ◽  
Binding Protein ◽  
Regulatory Element ◽  
Combined Therapy ◽  
High Fat ◽  
Fatty Acid Binding ◽  
Cornus Officinalis

Medicinal plants have been used worldwide as primary alternative healthcare supplements. Cornus officinalis (CO) and Ribes fasciculatum (RF) are traditional medicinal plants applied in East Asia to treat human diseases such as hepatitis, osteoporosis, oxidative stress and allergy. The aim of this study was to examine the anti-obesity effect of CO and RF on preadipocyte 3T3-L1 cells in vitro and high-fat diet (HFD)-induced obesity mice in vivo. Combination treatment of CO and RF in differentiated 3T3-L1 cells inhibited adipocyte differentiation through downregulation of adipogenesis-associated genes such as CCAAT/enhancer-binding protein alpha (Cebpa), fatty acid binding protein 4 (Fabp4), peroxisome proliferator-activated receptor gamma (Pparg) and sterol regulatory element binding protein (Srebp1). In vivo animal models showed that a mixture of CO and RF inhibited HFD-induced weight gain, resulting in decreased abdominal visceral fat tissues and fatty hepatocyte deposition. In addition, CO+RF treatment decreased HFD-induced adipogenesis-associated genes in abdominal white fat tissue. These results suggest that administration of a CO and RF mixture prevented adipocyte differentiation and lipid accumulation in preadipocyte cells and HFD-induced body weight in obesity mice. Therefore, combined therapy of CO and RF may be a protective therapeutic agent against obesity.

scholarly journals Antiobesity activity of Acer tegmentosum Maxim on 3T3-L1 preadipocyte and high-fat diet-induced obese rats

2020 ◽  
Author(s):  
Hang-Hee Cho ◽  
Soo-Jung Lee ◽  
Sung-Ho Kim ◽  
Sun-Hee Jang ◽  
Chungkil Won ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Adipocyte Differentiation ◽  
Binding Protein ◽  
High Fat ◽  
Tissue Mass ◽  
Fatty Acid Binding ◽  
Obese Rats

Abstract Background: The aim of this study was to investigate the effect of Acer tegmentosum Maxim (ATM) on adipocyte differentiation in 3T3-L1 adipocyte-derived cells and anti-obesity properties in high fat diet (HFD)-induced obese rats. Methods: 3T3-L1 adipocytes and HFD-induced obese rats were treated with ATM, and its effect on gene expression was analyzed using RT-PCR and Western blotting experiments. Results: Cellular lipid contents in DMI (dexamethasone, 3-isobutyl-1-methylxanthine, and insulin mixture)-treated cells increased, while ATM treatment caused a significant reduction in lipid accumulation in differentiated 3T3-L1 cells. ATM caused inhibition of adipogenesis via down-regulation of the CCAAT/enhancer binding protein β (C/EBPβ), C/EBPα, and peroxisome proliferator-activated receptor γ (PPARγ) expressions in 3T3-L1 cells. Moreover, treatment with ATM caused a decrease in the expressions of adipocyte-specific genes, such as adipocyte fatty acid-binding protein-2 (aP2), fatty acid synthase (FAS), and lipoprotein lipase (LPL), compared with DMI-stimulated adipocytes. In addition, phosphorylation levels of protein kinase B (Akt) and its downstream substrate, glycogen synthase kinase 3β (GSK3β), were significantly decreased by ATM treatment of 3T3-L1 adipocytes. Together, these results indicated that ATM caused inhibition of both adipocyte differentiation via suppression of the C/EBP family and PPARγ expressions and the Akt signaling pathway in 3T3-L1 adipocytes. In the present study, we further investigated anti-obesity effects of ATM on HFD-induced obese rats. Rats fed with HFD demonstrated elevations in body weight gain, while the administration of ATM significantly reversed BW gains and adipose tissue weights in rats fed HFD. ATM supplementation also caused a decrease in the circulating triglyceride levels and total cholesterol levels and led to inhibition of lipid accumulation in the adipose tissues in HFD-induced obesity in rats. Furthermore, epididymal fat exhibited larger adipocytes in the HFD group, whereas the ATM-treated group was significantly smaller than that of HFD group. These results strongly demonstrate that ATM administration caused a reduction in adiposity via attenuation in adipose tissue mass and adipocyte size. Conclusion: These finding demonstrated that ATM exerted anti-obesity effects through inhibition of adipocyte differentiation and adipogenesis, leading to a decrease in BW and fat tissue mass in HFD-induced obesity in rats.

scholarly journals The Correlation between MicroRNA-199a and White Adipose Tissue in C57/BL6J Mice with High-Fat Diet

2017 ◽  
Author(s):  
Dan Liu ◽  
Xia Wang ◽  
Xinying Lin ◽  
Baihui Zhang ◽  
Shue Wang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Therapeutic Potential ◽  
Binding Protein ◽  
Regulatory Element ◽  
Control Group ◽  
Model Group ◽  
High Fat ◽  
Fatty Acid Binding

AbstractUnderstanding is emerging about microRNAs as mediators in the regulation of white adipose tissue (WAT) and obesity. The expression level of miR-199a in mice was investigated to test our hypothesis: miR-199a might be related to fat accumulation and try to find its target mRNA, which perhaps could propose strategies with a therapeutic potential affecting the fat storage. C57/BL6J mice were randomly assigned to either a control group or an obesity model group (n=10 in both groups). Control mice were fed a normal diet (fat: 10 kcal %) ad libitum for 12 weeks, and model mice were fed a high-fat diet (fat: 30 kcal %) ad libitum for 12 weeks to induce obesity. At the end of the experiment, body fat mass and the free fatty acids (FFAs) and triglycerides (TGs) in WAT were tested. Fat cell size was measured by hematoxylin-eosin (H&E) staining method. The fat mass of the model group was higher than that of the control group (P<0.05). In addition, the concentrations of the FFAs and TGs were higher (P<0.05) and the adipocyte count was lower (P<0.05) in the model group. We tested the expression levels of miR-199a and key adipogenic transcription factors, including peroxisome proliferator activated receptor gamma2 (PPARγ2), CCAAT/enhancer binding proteins alpha (C/EBPα), adipocyte fatty acid-binding protein (aP2), and sterol regulatory element binding protein-1c (SREBP-1c). Up-regulated expression of miR-199a was observed in model group. Increased levels of miR-199a was accompanied by high expression levels of SREBP-1c. We found that the 3’-UTR of SREBP-1c mRNA has a predicted binding site for miR-199a. Based on the current discoveries, we suggest that miR-199a may exert its action by binding to its target mRNA and cooperate with SREBP-1c to induce obesity. Therefore, if the predicted binding site is confirmed by further research, miR-199a may have therapeutic potential for obesity.AbbreviationsWAT, white adipose tissue; PPARγ2, peroxisome proliferator, activated receptor γ2; C/EBP αCCAAT/enhancer binding proteins α; aP2, adipocyte fatty acid-binding protein; SREBP-1c, sterol regulatory element binding protein-1c; HFD, high-fat diet.

scholarly journals 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

2017 ◽  
Vol 117 (5) ◽  
pp. 645-661 ◽  
Author(s):  
Jyoti Gautam ◽  
Vikram Khedgikar ◽  
Priyanka Kushwaha ◽  
Dharmendra Choudhary ◽  
Geet Kumar Nagar ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Bone Loss ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Binding Protein ◽  
Regulatory Element ◽  
Adipogenic Differentiation ◽  
High Fat ◽  
Amp Activated Protein Kinase

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.

Analysis of Sterol-Regulatory Element-Binding Protein 1c Target Genes in Mouse Liver during Aging and High-Fat Diet

2013 ◽  
Vol 6 (2) ◽  
pp. 107-122 ◽  
Author(s):  
Frédéric Capel ◽  
Gaëlle Rolland-Valognes ◽  
Catherine Dacquet ◽  
Manuel Brun ◽  
Michel Lonchampt ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Mouse Liver ◽  
Target Genes ◽  
Binding Protein ◽  
Regulatory Element ◽  
High Fat ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

scholarly journals Oleacein Prevents High Fat Diet-Induced A Diposity and Ameliorates Some Biochemical Parameters of Insulin Sensitivity in Mice

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1829 ◽  
Author(s):  
Lepore ◽  
Maggisano ◽  
Bulotta ◽  
Mignogna ◽  
Arcidiacono ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
High Fat Diet ◽  
Fatty Acid Synthase ◽  
Glucose Transporter ◽  
Regulatory Element ◽  
Regulatory Elements ◽  
High Fat

Oleacein is one of the most abundant polyphenolic compounds of olive oil, which has been shown to play a protective role against several metabolic abnormalities, including dyslipidemia, insulin resistance, and glucose intolerance. Herein, we investigated the effects of oleacein on certain markers of adipogenesis and insulin-resistance in vitro, in 3T3-L1 adipocytes, and in vivo in high-fat diet (HFD)-fed mice. During the differentiation process of 3T3-L1 preadipocytes into adipocytes, oleacein strongly inhibited lipid accumulation, and decreased protein levels of peroxisome proliferator-activated receptor gamma (PPARγ) and fatty acid synthase (FAS), while increasing Adiponectin levels. In vivo, treatment with oleacein of C57BL/6JOlaHsd mice fed with HFD for 5 and 13 weeks prevented the increase in adipocyte size and reduced the inflammatory infiltration of macrophages and lymphocytes in adipose tissue. These effects were accompanied by changes in the expression of adipose tissue-specific regulatory elements such as PPARγ, FAS, sterol regulatory element-binding transcription factor-1 (SREBP-1), and Adiponectin, while the expression of insulin-sensitive muscle/fat glucose transporter Glut-4 was restored in HFD-fed mice treated with oleacein. Collectively, our findings indicate that protection against HFD-induced adiposity by oleacein in mice is mediated by the modulation of regulators of adipogenesis. Protection against HFD-induced obesity is effective in improving peripheral insulin sensitivity.

scholarly journals Coumarin attenuates hepatic steatosis by down-regulating lipogenic gene expression in mice fed a high-fat diet

2013 ◽  
Vol 109 (9) ◽  
pp. 1590-1597 ◽  
Author(s):  
Min Young Um ◽  
Mi Kyeong Moon ◽  
Jiyun Ahn ◽  
Tae Youl Ha
Keyword(s):  
Gene Expression ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Fatty Acid Synthase ◽  
Binding Protein ◽  
Regulatory Element ◽  
Thiobarbituric Acid Reactive Substance ◽  
High Fat ◽  
Lipogenic Gene ◽  
Lipogenic Gene Expression

Coumarin is a natural compound abundant in plant-based foods such as citrus fruits, tomatoes, vegetables and green tea. Although coumarin has been reported to exhibit anti-coagulant, anti-inflammation and cholesterol-lowering properties, the effect of coumarin on hepatic lipid metabolism remains unclear. In the present study, we evaluated the ability of coumarin to protect against hepatic steatosis associated with a high-fat diet (HFD) and investigated potential mechanisms underlying this effect. C57BL/6J mice were fed a normal diet, HFD and HFD containing 0·05 % courmarin for 8 weeks. The present results showed that coumarin reduced weight gain and abdominal fat mass in mice fed the HFD for 8 weeks (P< 0·05). Coumarin also significantly reduced the HFD-induced elevation in total cholesterol, apoB, leptin and insulin (P< 0·05). In the liver of HFD-fed mice, coumarin significantly reduced total lipids, TAG and cholesterol (38, 22 and 9 % reductions, respectively; P< 0·05), as well as lipid droplet number and size. Additionally, thiobarbituric acid-reactive substance levels, as an indicator of hepatic steatosis, were attenuated by coumarin (P< 0·05). Finally, coumarin suppressed the HFD-induced up-regulation in fatty acid synthase (FAS) activity, and the expression of sterol regulatory element-binding protein-1, FAS, acetyl-CoA carboxylase 1, PPARγ and CCAAT/enhancer-binding protein-α in the liver. Taken together, these results demonstrate that coumarin could prevent HFD-induced hepatic steatosis by regulating lipogenic gene expression, suggesting potential targets for preventing hepatic steatosis.

scholarly journals Cellular Retinol-Binding Protein Type I (CRBP-I) Regulates Adipogenesis

2010 ◽  
Vol 30 (14) ◽  
pp. 3412-3420 ◽  
Author(s):  
C. F. Zizola ◽  
S. K. Frey ◽  
S. Jitngarmkusol ◽  
B. Kadereit ◽  
N. Yan ◽  
...  
Keyword(s):  
Transcription Factors ◽  
High Fat Diet ◽  
Adipocyte Differentiation ◽  
Binding Protein ◽  
Retinol Binding Protein ◽  
Type I ◽  
High Fat ◽  
Embryonic Fibroblasts ◽  
Glucose Tolerant ◽  
Cellular Retinol Binding Protein

ABSTRACT Adipogenesis is governed by a well-documented cascade of transcription factors. However, less is known about non-transcription factors that govern early stages of adipogenesis. Here we show that cellular retinol-binding protein type I (CRBP-I), a small cytosolic binding protein for retinol and retinaldehyde, is specifically restricted to preadipocytes in white adipose tissue. The absence of CRBP-I in mice (CRBP-I-KO mice) leads to increased adiposity. Despite increased adiposity, CRBP-I-KO mice remain more glucose tolerant and insulin sensitive during high-fat-diet feeding. 3T3-L1 cells deficient in CRBP-I or mouse embryonic fibroblasts derived from CRBP-I-KO mice had increased adipocyte differentiation and triglyceride (TG) accumulation. This was due to increased expression and activity of PPARγ, while other transcription factor pathways in early and late differentiation remained unchanged. Conversely, the overexpression of CRBP-I in 3T3-L1 cells results in decreased TG accumulation. In conclusion, CRBP-I is a cytosolic protein specifically expressed in preadipocytes that regulates adipocyte differentiation in part by affecting PPARγ activity.

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