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 Systemic Overexpression of GDF5 in Adipocytes but Not Hepatocytes Alleviates High-Fat Diet-Induced Nonalcoholic Fatty Liver in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yan Yang ◽  
Wenting Zhang ◽  
Xiaohui Wu ◽  
Jing Wu ◽  
Chengjun Sun ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Lentiviral Vector ◽  
Cell Model ◽  
Control Group ◽  
High Fat ◽  
Fatty Acid Binding ◽  
Nonalcoholic Fatty Liver

Objective. Our recent study demonstrated that growth differentiation factor 5 (GDF5) could promote white adipose tissue thermogenesis and alleviate high-fat diet- (HFD-) induced obesity in fatty acid-binding protein 4- (Fabp4-) GDF5 transgenic mice (TG). Here, we further investigated the effects of systemic overexpression of the GDF5 gene in adipocytes HFD-induced nonalcoholic fatty liver disease (NAFLD). Methods. Fabp4-GDF5 TG mice were administered an HFD feeding. NAFLD-related indicators associated with lipid metabolism and inflammation were measured. A GDF5 lentiviral vector was constructed, and the LO2 NAFLD cell model was induced by FFA solution (oleic acid and palmitic acid). The alterations in liver function, liver lipid metabolism, and related inflammatory indicators were analyzed. Results. The liver weight was significantly reduced in the TG group, which was in accordance with the significantly downregulated expression of TNFα, MCP1, Aim2, and SREBP-1c and significantly upregulated expression of CPT-1α and ACOX2 in TG mouse livers. Compared to that of cells in the FAA-free control group, LO2 cells with in situ overexpression of GDF5 developed lipid droplets after FFA treatment; the levels of triglycerides, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were significantly increased in both the GDF5 lentivirus and control lentivirus groups compared with those of the FAA-free group. Additionally, the levels of FAS, SREBP-1, CPT-1α, and inflammation-associated genes, such as ASC and NLRC4, were unaltered despite GDF5 treatment. Conclusion. Systemic overexpression of GDF5 in adipose tissue in vivo significantly reduced HFD-induced NAFLD liver damage in mice. The overexpression of GDF5 in hepatocytes failed to improve lipid accumulation and inflammation-related reactions induced by mixed fatty acids, suggesting that the protective effect of GDF5 in NAFLD was mainly due to the reduction in adipose tissue and improvements in metabolism. Hence, our study suggests that the management of NAFLD should be targeted to reduce the overall amount of body fat and improve metabolic status before the progression to nonalcoholic steatohepatitis occurs.

scholarly journals PO-043 The Effects of One-Time High Intensity Intermittent Training on Expression of LC3 Gene in Rats’ White Adipose Tissue

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Qishu Zhou ◽  
Chunyu Liang ◽  
Yafei Li ◽  
Yi Yan
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Intensity ◽  
High Fat Diet ◽  
Intermittent Exercise ◽  
Diet Group ◽  
Control Group ◽  
High Fat ◽  
Subcutaneous White Adipose Tissue ◽  
White Fat

Objective  To investigate the effect of one-time high-intensity intermittent exercise in white fat autophagy in obese rats and provide a theoretical basis of the molecular mechanism of exercise fat loss. Methods  Eighteen male 3-weeks-old rats were selected and divided into control group fed with normal diet (C), high-fat diet group fed with high fat diet (H). After 16 weeks, there were twelve obesity rats that divided into diet group (HS) and exercise group (HE). The other six control group rats of 19 weeks age were used as the standard (CS group). OE group did the high intensity intermittent exercise once. The CS group and the CS group were kept quietly. Three groups were taken subcutaneous white adipose tissue(S) and epididymal white adipose tissue (E) immediately after exercise. Mensurate the expression of LC3 gene in the tissue using the fluorescent quantitative PCR. Results 1. The expression of LC3 mRNA from white fat tissue was different to the tissues, which the expression of epididymal white adipose tissue of each group was higher than that in subcutaneous white adipose tissue (P <0.01). 2. Compared with CS group, the expression of epididymal white fat adipose tissue LC3 mRNA decreased (P<0.01) and the expression of the subcutaneous white adipose tissue increased from HS group (P <0.05). 3. Compared with OS group, the expression of epididymal white fat adipose tissue LC3 mRNA decreased (P<0.05) and the expression of subcutaneous white adipose tissue decreased from OS group. Conclusions The expression of LC3mRNA in epididymal white fat adipose tissue of rats was significantly higher than that of subcutaneous white fat. The changes of LC3mRNA expression of adipose tissue caused by high-fat diet have tissue differences. One-time high-intensity intermittent exercise can reduce the expression of LC3mRNA in fat tissue of obese rats. Its regulatory mechanism needs to be further studied.

scholarly journals Electroacupuncture Decreases the Leukocyte Infiltration to White Adipose Tissue and Attenuates Inflammatory Response in High Fat Diet-Induced Obesity Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Chorng-Kai Wen ◽  
Tzung-Yan Lee
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Response ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Target Genes ◽  
Inflammatory Responses ◽  
Regulatory Element ◽  
Epididymal Adipose Tissue ◽  
High Fat ◽  
Obese Rats

Suppression of white adipose tissue inflammatory signaling may contribute to the pathogenesis of obesity-induced inflammatory response. However, the precise mechanism of efficacy of acupuncture related to adipose tissue remains poorly understood. In the present study we evaluated the anti-inflammatory activities of 10 Hz electroacupuncture (EA) which was applied at the acupoint Zusanli (ST36) for 20 min per day in high-fat diet- (HFD-) induced obesity model. Treatment lasted for one week. Obese rats treated with EA showed significantly reduced body weight compared with the rats in HFD group. EA decreased the number of F4/80 and CD11b-positive macrophages in epididymal adipose tissue. We found that 10 Hz EA given 7 days/week at ST36 acupoints significantly alleviated macrophage recruitment and then improved the obesity-associated factors of sterol regulatory element-binding protein-1 (SREBP-1) and target genes expression in rats with HFD. Adipose tissue inflammatory responses indicated by tumor necrosis factor-α(TNF-α), IL-6, monocyte chemotactic protein-1 (MCP-1), and CD68 mRNA expression were significantly reduced by EA in obese rats. Additionally, EA was found to significantly reduced serum levels of TNF-α, IL-6, and IL-1 in this model. These results indicated that EA improved adipose tissue inflammatory response in obese rats, at least partly, via attenuation of lipogenesis signaling.

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 Lyophilized Maqui (Aristotelia chilensis) Berry Induces Browning in the Subcutaneous White Adipose Tissue and Ameliorates the Insulin Resistance in High Fat Diet-Induced Obese Mice

Antioxidants ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 360 ◽  
Author(s):  
Viviana Sandoval ◽  
Antoni Femenias ◽  
Úrsula Martínez-Garza ◽  
Hèctor Sanz-Lamora ◽  
Juan Castagnini ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Binding Protein ◽  
Fibroblast Growth Factor 21 ◽  
Obese Mice ◽  
High Fat ◽  
Subcutaneous White Adipose Tissue ◽  
Aristotelia Chilensis

Maqui (Aristotelia Chilensis) berry features a unique profile of anthocyanidins that includes high amounts of delphinidin-3-O-sambubioside-5-O-glucoside and delphinidin-3-O-sambubioside and has shown positive effects on fasting glucose and insulin levels in humans and murine models of type 2 diabetes and obesity. The molecular mechanisms underlying the impact of maqui on the onset and development of the obese phenotype and insulin resistance was investigated in high fat diet-induced obese mice supplemented with a lyophilized maqui berry. Maqui-dietary supplemented animals showed better insulin response and decreased weight gain but also a differential expression of genes involved in de novo lipogenesis, fatty acid oxidation, multilocular lipid droplet formation and thermogenesis in subcutaneous white adipose tissue (scWAT). These changes correlated with an increased expression of the carbohydrate response element binding protein b (Chrebpb), the sterol regulatory binding protein 1c (Srebp1c) and Cellular repressor of adenovirus early region 1A–stimulated genes 1 (Creg1) and an improvement in the fibroblast growth factor 21 (FGF21) signaling. Our evidence suggests that maqui dietary supplementation activates the induction of fuel storage and thermogenesis characteristic of a brown-like phenotype in scWAT and counteracts the unhealthy metabolic impact of an HFD. This induction constitutes a putative strategy to prevent/treat diet-induced obesity and its associated comorbidities.

scholarly journals The Antiobesity Effects of Buginawa in 3T3-L1 Preadipocytes and in a Mouse Model of High-Fat Diet-Induced Obesity

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Yea-Jin Park ◽  
Dong-Wook Seo ◽  
Jae-Yun Ju ◽  
Yun-Yeop Cha ◽  
Hyo-Jin An
Keyword(s):  
Adipose Tissue ◽  
Mouse Model ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Liver Tissue ◽  
Binding Protein ◽  
Medicinal Herbs ◽  
High Fat ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

There has been a remarkable interest in finding lipid inhibitors from natural products to replace synthetic compounds, and a variety of oriental medicinal herbs are reported to have biological activity with regard to lipid inhibition. Buginawa (Bugi) is a novel combined formula that contains twelve medicinal herbs with potential for weight loss induction. We hypothesized that Bugi may have antiobesity effects in 3T3-L1 preadipocytes and in a high-fat diet- (HFD-) induced mouse model. In this study, 3T3-L1 cells were treated with varied concentrations of Bugi (62.5, 125, or 250 μg/mL). Bugi treatment inhibited adipocyte differentiation by suppressing adipogenic transcription genes, including peroxisome proliferator-activated receptor γ protein (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα), sterol regulatory element-binding protein 1 (SREBP1), and CCAAT/enhancer-binding protein β (C/EBPβ). Mice were fed a normal diet or an HFD for 11 weeks, and Bugi was simultaneously administered at 50 or 100 mg/kg. Bugi administration significantly reduced body weight gain and white adipose tissue (WAT) weight and effectively inhibited lipid droplet accumulation in epididymal white adipose tissue (eWAT) and liver tissue. Further, Bugi treatment suppressed mRNA levels of PPARγ, C/EBPα, and SREBP1 in eWAT and liver tissue. Our findings demonstrate that Bugi could be an effective candidate for preventing obesity and related metabolic disorders.

scholarly journals Body Composition Changes in Female APOE*3Leiden.CETP Transgenic Mice After 5-week Injection of Resveratrol-encapsulated Liposomes to Inguinal White Adipose Tissue (P21-041-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Zeynep Goktas ◽  
Md Shahjalal Hossain Khan ◽  
Yujiao Zu ◽  
Lei Hao ◽  
Shu Wang
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Transgenic Mice ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Saline Control ◽  
Control Group ◽  
High Fat

Abstract Objectives Many cell culture and animal studies have demonstrated that Trans-resveratrol (R) has the potential to induce beige cell formation and activity. Although human studies indicate that R can maintain metabolic health, evidence is inconclusive regarding its browning effectiveness mainly due to its low aqueous solubility and high hepatic metabolism in humans. To combat the shortcomings of R, we have successfully synthesized biocompatible and biodegradable R-encapsulated liposomes (Rlipo). We will directly inject Rlipo into inguinal white adipose tissue (iWAT) in this project. The purpose of this study to evaluate the anti-obesity effects of resveratrol-encapsulated liposomes in female APOE*3Leiden.CETP transgenic mice, which have human-like lipoprotein metabolism. Methods Rlipo was prepared using R and soy phosphatidylcholine (soy-PC) dissolved in ethanol. After mixing and drying with nitrogen, deionized water was added followed by a sonication step. Ultrafiltration was used to remove any unencapsulated R. The void liposomes (Vlipo) were prepared using only soy-PC. Female APOE*3Leiden.CETP mice (n = 40) were fed with a high fat diet (45% of calorie from fat) throughout the study. After 4 weeks of the high-fat diet administration, mice were randomly divided into 4 groups (n = 10) and received iWAT injections of Rlipo, Vlipo, free R and saline (control) once per week for 5 weeks. R concentration was 17.5 mg/kg body weight/week. Body weight and food intake were measured weekly. Body composition of mice was measured using an EchoMRITM every other week. Paired sample t-test and One-way ANOVA were used to analyze differences between means. Results After 5-weeks of treatment compared to baseline, fat percentage differences were 1.99 ± 0.93%, 1.85 ± 0.58%, 1.45 ± 0.67%, and 1.40 ± 0.68% in control, free R, Vlipo and Rlipo groups, respectively. Body weight and fat mass showed a similar trend of change. Although control group showed an increase in lean mass (0.25 ± 0.95 g), RLipo group showed a decrease (−0.14 ± 0.52 g). Food intake was similar among four groups. Conclusions Nanoencapsulation of R can enhance R's anti-obesity effects. However longer treatment time might be necessary to see more prominent results. Funding Sources NIH/NCCIH (Grant R15AT008733).

scholarly journals Acer tegmentosum Maxim Inhibits Adipogenesis in 3t3-l1 Adipocytes and Attenuates Lipid Accumulation in Obese Rats Fed a High-Fat Diet

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3753
Author(s):  
Hang-Hee Cho ◽  
Soo-Jung Lee ◽  
Sung-Ho Kim ◽  
Sun-Hee Jang ◽  
Chungkil Won ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Fatty Acid Synthase ◽  
Binding Protein ◽  
High Fat ◽  
Fatty Acid Binding ◽  
Obese Rats

We investigated the effect of Acer tegmentosum Maxim (ATM) on adipocyte differentiation in 3T3-L1 cells and anti-obesity properties in obese rats fed a high-fat diet (HFD). Cellular lipid content 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 (60 ug/mL) caused inhibition of adipogenesis via down-regulation of the CCAAT/enhancer binding protein β (C/EBPβ) (48%), C/EBPα (66%), and peroxisome proliferator-activated receptor γ (PPARγ) (64%) expressions in 3T3-L1 cells. Moreover, ATM induced 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). Protein kinase B (Akt) and glycogen synthase kinase 3β (GSK3β) phosphorylation was also decreased by ATM treatment of 3T3-L1 adipocytes. We investigated the anti-obesity effects of ATM on HFD-induced obese rats. Rats fed with an HFD demonstrated elevations in body weight gain, while the administration of ATM reversed body weight (BW) gains and adipose tissue weights in rats fed an HFD. ATM supplementation caused a decrease in the circulating triglyceride and total cholesterol levels and led to inhibition of lipid accumulation in the adipose tissues in HFD-induced obese rats. Epididymal fat exhibited significantly larger adipocytes in the HFD group than it did in the ATM-treated group. These results demonstrate that ATM administration caused a reduction in adiposity via attenuation in adipose tissue mass and adipocyte size.

scholarly journals The effect of aerobic exercise training on gene expression of beta3-adrenergic receptor and beta-arrestin2 in inguinal white adipose tissue of mice fed with a high fat diet

2021 ◽  
Vol 23 (3) ◽  
pp. 124-130
Author(s):  
Saeed Daneshyar ◽  
Mehdi Bahmani ◽  
Yazdan Fourotan
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Adrenergic Receptor ◽  
Aerobic Training ◽  
Control Group ◽  
Preventive Effect ◽  
High Fat ◽  
Adrenergic Signaling

Background and aims: Beta-adrenergic signaling deficiency has been established to be related to obesity and related diseases. Beta3- adrenergic receptor (Adrb3) and beta-arrestin2 (Barr2) are pivotal agents in the beta-adrenergic-signaling pathway. This study aimed to investigate the preventive effect of aerobic training on dysregulation of Adrb3 and Barr2 gene expression that was induced by high-fat diet (HFD) in inguinal white adipose tissue of mice. Materials and Methods: Twenty-one C57BL/6 mice were assigned to three groups as follows: 1) control group (n=7), 2) high-fat diet-induced overweight (HFD-OW) (n=7), and 3) high-fat diet with aerobic training (HFD-AT) (n=7). The HFD-OW group were fed with a HFD for 12 weeks. The HFD-AT group had aerobic training for six weeks on a treadmill in addition to feeding with the HFD. The real-time polymerase chain reaction (PCR) method was used to measure the gene expression of Adrb3 and Barr2 in inguinal white adipose tissue. Results: The gene expression of Adrb3 did not significantly change between groups (P>0.05). However, the expression of Barr2 in HFD-OW group was significantly increased as compared to the control group (1.5-fold: P=0.001). Interestingly, the Barr2 expression in HFD-AT group was significantly lower compared with HFD-OW group (P=0.045). Conclusion: The results indicated that aerobic training could inhibit the upregulation of Barr2 induced by HFD. It seems that a portion of the preventive effect of aerobic training on the development of obesity may be mediated by inhibiting the Barr2 expression in adipose tissue.

Expression of the key metabolic regulators in the white adipose tissue of rats; the role of high-fat diet and aerobic training

2018 ◽  
Vol 14 (4) ◽  
pp. 271-277 ◽  
Author(s):  
M. Ebrahimi ◽  
R. Fathi ◽  
Z. Ansari Pirsaraei ◽  
E. Talebi-Garakani ◽  
M. Najafi
Keyword(s):  
Adipose Tissue ◽  
Lipid Profile ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Aerobic Training ◽  
Regulatory Element ◽  
Farnesoid X Receptor ◽  
Weight Changes ◽  
High Fat ◽  
Male Wistar Rats

Lipid metabolism, especially in the white adipose tissue as an active metabolic organ, is tightly regulated by the key transcription factors, such as the sterol regulatory element binding protein 1c (SREBP-1c) and the Farnesoid X Receptor (FXR). We have studied the expression of these genes in the white adipose tissue to see how a high fat diet (HFD) and two intensities of aerobic training change the lipogenic and lipolytic pathways. 44 male Wistar rats randomly divided into the normal (12% calories from fat) and HFD (56% calories from fat) groups. Each group included control (n=6), moderate trained (n=8, ~65% Vo2max) and high intensity trained (n=8, ~75% Vo2max) rats. After 8 weeks of training, the weight changes, plasma insulin and lipid profile levels and the relative gene expression of SREBP-1c and FXR in the adipose tissue was measured. Data were analysed by 2-way ANOVA (P<0.05). HFD fed rats showed higher levels of insulin and dyslipidemia that was correlated with the higher weight gain. Also, the adipose expression of SREBP-1c was higher in the HFD fed rats that it was strongly correlated with the lower FXR expression. Trained rats independent of the intensity of the training showed lower SREBP-1c and higher FXR expression, but no change was observed in the lipid profile levels. HFD-induced dyslipidemia could occur via SREBP-1c activation in the adipose tissue while the aerobic training activates FXR and inhibits the lipogenic pathways. Despite the activation of lipolytic pathways in the trained rats, it seems that diet has more effect on the lipid profile than the aerobic training.

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