scholarly journals Anti-Obesity Effect of Extract from Nelumbo Nucifera L., Morus Alba L., and Raphanus Sativus Mixture in 3T3-L1 Adipocytes and C57BL/6J Obese Mice

Foods ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 170 ◽  
Author(s):  
Wan-Sup Sim ◽  
Sun-Il Choi ◽  
Bong-Yeon Cho ◽  
Seung-Hyun Choi ◽  
Xionggao Han ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Raphanus Sativus ◽  
Ethanol Extract ◽  
Morus Alba ◽  
Nelumbo Nucifera ◽  
Total Phenolic ◽  
Control Group ◽  
High Fat

The antioxidant and anti-adipogenic activities of a mixture of Nelumbo nucifera L., Morus alba L., and Raphanus sativus were investigated and their anti-obesity activities were established in vitro and in vivo. Among the 26 different mixtures of extraction solvent and mixture ratios, ethanol extract mixture no. 1 (EM01) showed the highest antioxidant (α,α-Diphenyl-β-picrylhydrazyl, total phenolic contents) and anti-adipogenic (Oil-Red O staining) activities. EM01 inhibited lipid accumulation in 3T3-L1 adipocytes compared to quercetin-3-O-glucuronide. Furthermore, body, liver, and adipose tissue weights decreased in the high-fat diet (HFD)-EM01 group compared to in the high-fat diet control group (HFD-CTL). EM01 lowered blood glucose levels elevated by the HFD. Lipid profiles were improved following EM01 treatment. Serum adiponectin significantly increased, while leptin, insulin growth factor-1, non-esterified fatty acid, and glucose significantly decreased in the HFD-EM01 group. Adipogenesis and lipogenesis-related genes were suppressed, while fat oxidation-related genes increased following EM01 administration. Thus, EM01 may be a natural anti-obesity agent.

scholarly journals Evaluation of anti-obesity potential of aqueous extract of Achyranthes aspera Linn. in high fat diet induced obese rats

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Kumaraswamy Athesh ◽  
Rangaraju Sivasubramanian ◽  
Gnanasekaran Jothi ◽  
Pemiah Brindha
Keyword(s):  
Aqueous Extract ◽  
Pancreatic Lipase ◽  
High Fat Diet ◽  
In Vivo Studies ◽  
Control Group ◽  
High Fat ◽  
Achyranthes Aspera ◽  
Obese Rats

Abstract Background Obesity, reached epidemic proportions globally is often associated with life threatening comorbidities. The unavailability of safe and effective long term medications for obesity in modern pharmacotherapy forces the scientific community to explore the potential of Ayurvedic traditional healers as they are considered safe and effective. Objective To explore the anti-obesity potential of aqueous extract of aerial parts of Achyranthes aspera L. (AEAA), a traditional healer in high fat diet (HFD) induced obese rats. Methods AEAA was prepared and subjected to in-vitro pancreatic lipase inhibition assay and in-vivo anti-obesity studies. For in-vivo studies, HFD fed obese prone Wistar albino rats were divided into five experimental groups (Group II to VI): animals fed with standard pellet chow served as normal control (Group I) while, animals continued with HFD alone served as obese control (Group II); Group III, IV and V were administered AEAA at a dose of 100, 200 and 300 mg/kg b.w. respectively along with HFD; and animals administered orlistat (30 mg/kg bw) along with HFD served as standard control (Group VI). All the drugs were administered orally once a day for a period of 60 days. At the end of the experimental period various physical, biochemical and histopathological observations were made. Results In-vitro studies showed AEAA partially but not significantly inhibited the activity of pancreatic lipase. Data of in-vivo studies revealed, significant reduction in body weights, fat pad weights and organ weights upon AEAA treatment. Elevated levels of glucose, insulin, leptin, lipid profiles and antioxidant status were also brought back to normal. Conclusion The obtained results clearly suggested that AEAA possess pronounced anti-obesity potential.

scholarly journals 3,3′-Diindolylmethane Dose-Dependently Prevents Advanced Prostate Cancer

2019 ◽  
Author(s):  
Yufei Li ◽  
Nathaniel W. Mahloch ◽  
Nicholas J.E. Starkey ◽  
Mónica Peña-Luna ◽  
George E. Rottinghaus ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
High Fat Diet ◽  
Estrogen Receptor Alpha ◽  
Estrogen Receptor Beta ◽  
Control Group ◽  
High Fat ◽  
Mouse Prostate

Abstract3,3′-Diindolylmethane (DIM) is an acid-derived dimer of indole-3-carbinol, found in many cruciferous vegetables, such as broccoli, and has been shown to inhibit prostate cancer (PCa) in several in vitro and in vivo models. We demonstrated that DIM stimulated both estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) transcriptional activities and propose that ERβ plays a role in mediating DIM’s inhibition on cancer cell growth. To further study the effects of DIM on inhibiting advanced PCa development, we tested DIM in TRAMP (TRansgenic Adenocarcinoma of the Mouse Prostate) mice. The control group of mice were fed a high fat diet. Three additional groups of mice were fed the same high fat diet supplemented with 0.04%, 0.2% and 1% DIM. Incidence of advanced PCa, poorly differentiated carcinoma (PDC), in the control group was 60%. 1% DIM dramatically reduced PDC incidence to 24% (p=0.0012), while 0.2% and 0.04% DIM reduced PDC incidence to 38% (p=0.047) and 45% (p=0.14) respectively. Though DIM did affect mice weights, statistical analysis showed a clear negative association between DIM concentration and PDC incidence with p=0.004, while the association between body weight and PDC incidence was not significant (p=0.953). In conclusion, our results show that dietary DIM can inhibit the most aggressive stage of prostate cancer at concentration lower than previously demonstrated, possibly working through an estrogen receptor mediated mechanism.

scholarly journals Assessment of Antiobesity Potential ofAchyranthes asperaLinn. Seed

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Neerja Rani ◽  
Surendra Kumar Sharma ◽  
Neeru Vasudeva
Keyword(s):  
Lipase Activity ◽  
High Fat Diet ◽  
Ethanol Extract ◽  
Phytochemical Analysis ◽  
Pancreatic Amylase ◽  
High Fat ◽  
Saponin Content ◽  
Plasma Triacylglycerol

The present study was designed to evaluate the quality control parameters, quantitative phytochemical analysis (total phenols, total flavonoids, and total saponin content), and the antiobesity effect of ethanol extract ofAchyranthes asperaLinn. seed (EAA) by employingin vitroandin vivomodels. Inin vitrostudy, the inhibitory activity of EAA on pancreatic amylase and lipase was measured. Thein vivopancreatic lipase activity was evaluated by measurement of plasma triacylglycerol levels after oral administration of EAA along with lipid emulsion to Swiss albino mice. The EAA inhibited pancreatic amylase and lipase activity in vitro and elevations of plasma triacylglycerol level in mice. Furthermore, the antiobesity effect of EAA (900 mg/kg) was assessed in mice fed a high-fat diet with or without EAA for 6 weeks. EAA significantly suppressed the increase in body,retroperitoneal adiposetissue, liver weights, and serum parameters, namely; total cholesterol, total triglyceride, and LDL-cholesterol level. The anti obesity effects of EAA in high-fat-diet-treated mice may be partly mediated through delaying the intestinal absorption of dietary fat by inhibiting pancreatic amylase and lipase activity. Histopathological effects of EAA on the liver of mice were also assessed.

scholarly journals Comparison of Efficacy of the Pap and H & E in Identifying the Various Changes in Liver Samples of High Fat Diet Induced Rat - In vitro Study

2021 ◽  
pp. 364-380
Author(s):  
E. Dhivya Sri ◽  
R. Priyadharshini ◽  
Palati Sinduja ◽  
V. Meghashree
Keyword(s):  
Metabolic Syndrome ◽  
High Fat Diet ◽  
In Vitro Study ◽  
Signs And Symptoms ◽  
Calorie Intake ◽  
Control Group ◽  
High Fat ◽  
Wide Range

Introduction: High fat induced (HFI) liver is associated with a high calorie intake and many other diet-induced complications, such as metabolic syndrome and cardiovascular disease. HFI is the most common chronic liver disease that develops due to high fat intake. A wide range of liver injuries is associated with HFI, ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), advanced fibrosis and cirrhosis. The signs and symptoms of metabolic syndrome may be induced in rats by feeding them a diet rich in carbohydrates and fat. The aim of the study is Comparison of efficacy of the PAP (Papanicolaou) stain and H&E (Hematoxylin and eosin) stain in identifying the various changes in liver samples of high fat diet induced rat. Materials and Methods: Liver samples of Normal control group animal and High fat diet induced animal were sectioned, weighed fixed 10% neutral buffer formalin and mounted in DPX compound. Four micrometer sections were stained with hematoxylin-eosin and PAP stains for the histological examination of micro-vesicular and macro-vesicular steatosis in the liver tissue. The grading of steatosis was given from 0-3 based on the lipid accumulation (steatosis): grade 0 - absence; grade 1 - mild Steatosis (<30% hepatocyte); grade 2- moderate steatosis (30%-70% hepatocyte); grade3- severe steatosis (>70%hepatocytes). Efficacy of grade of PAP stain and H&E stain were accessed and statistically evaluated by considering seven parameters and overall staining characters where compared. Results: Our present study evaluated high fat induced hepatic steatosis of H&E and PAP stain and also evaluated efficacy of both the stain. In our study, Pie chart showing the percentage distribution of Number of micro-vesicles about 70% represents greater than 30, 10% represents 30-70, 20% represents less than 70 (Fig. 1). In our study 20% represents the greater than 30, 30% represents the 30-70, 50% represents Less than 70 (Fig. 2). 30% represents mild steatosis, 20% represents moderate steatosis, 50% represents Severe Steatosis (Fig. 3).           Conclusion: We demonstrated the comparative efficiency of the PAP and H&E high fat diet induced rat liver by in vivo and conclude that both H&E and PAP stain has equal efficacy and clarity in observing the various minute parameters.

Sequoyitol ameliorates diabetic nephropathy in diabetic rats induced with a high-fat diet and a low dose of streptozotocin

2014 ◽  
Vol 92 (5) ◽  
pp. 405-417 ◽  
Author(s):  
Xian-Wei Li ◽  
Yan Liu ◽  
Wei Hao ◽  
Jie-Ren Yang
Keyword(s):  
Diabetic Nephropathy ◽  
Blood Glucose ◽  
High Fat Diet ◽  
Low Dose ◽  
Serum Insulin ◽  
Fasting Blood Glucose ◽  
Diabetic Rats ◽  
High Fat

Sequoyitol decreases blood glucose, improves glucose intolerance, and enhances insulin signaling in ob/ob mice. The aim of this study was to investigate the effects of sequoyitol on diabetic nephropathy in rats with type 2 diabetes mellitus and the mechanism of action. Diabetic rats, induced with a high-fat diet and a low dose of streptozotocin, and were administered sequoyitol (12.5, 25.0, and 50.0 mg·(kg body mass)−1·d−1) for 6 weeks. The levels of fasting blood glucose (FBG), serum insulin, blood urea nitrogen (BUN), and serum creatinine (SCr) were measured. The expression levels of p22phox, p47phox, NF-κB, and TGF-β1 were measured using immunohistochemisty, real-time PCR, and (or) Western blot. The total antioxidative capacity (T-AOC), as well as the levels of malondialdehyde (MDA) and reactive oxygen species (ROS) were also determined. The results showed that sequoyitol significantly decreased FBG, BUN, and SCr levels, and increased the insulin levels in diabetic rats. The level of T-AOC was significantly increased, while ROS and MDA levels and the expression of p22phox, p47phox, NF-κB, and TGF-β1 were decreased with sequoyitol treatment both in vivo and in vitro. These results suggested that sequoyitol ameliorates the progression of diabetic nephropathy in rats, as induced by a high-fat diet and a low dose of streptozotocin, through its glucose-lowering effects, antioxidant activity, and regulation of TGF-β1 expression.

scholarly journals Aloe-Emodin Relieves High-Fat Diet Induced QT Prolongation via MiR-1 Inhibition and IK1 Up-Regulation in Rats

2017 ◽  
Vol 43 (5) ◽  
pp. 1961-1973 ◽  
Author(s):  
Yan Bai ◽  
Zhenli Su ◽  
Hanqi Sun ◽  
Wei Zhao ◽  
Xue Chen ◽  
...  
Keyword(s):  
Action Potential ◽  
Protein Expression ◽  
High Fat Diet ◽  
Qt Prolongation ◽  
Electrical Remodeling ◽  
High Fat ◽  
Treatment Groups ◽  
Aloe Emodin

Background/Aims: High-fat diet (HFD) causes cardiac electrical remodeling and increases the risk of ventricular arrhythmias. Aloe-emodin (AE) is an anthraquinone component isolated from rhubarb and has a similar chemical structure with emodin. The protective effect of emodin against cardiac diseases has been reported in the literature. However, the cardioprotective property of AE is still unknown. The present study investigated the effect of AE on HFD-induced QT prolongation in rats. Methods: Adult male Wistar rats were randomly divided into three groups: control, HFD, and AE-treatment groups. Normal diet was given to rats in the control group, high-fat diet was given to rats in HFD and AE-treatment groups for a total of 10 weeks. First, HFD rats and AE-treatment rats were fed with high-fat diet for 4 weeks to establish the HFD model. Serum total cholesterol and triglyceride levels were measured to validate the HFD model. Afterward, AE-treatment rats were intragastrically administered with 100 mg/kg AE each day for 6 weeks. Electrocardiogram monitoring and whole-cell patch-clamp technique were applied to examine cardiac electrical activity, action potential and inward rectifier K+ current (IK1), respectively. Neonatal rat ventricular myocytes (NRVMs) were subjected to cholesterol and/or AE. Protein expression of Kir2.1 was detected by Western blot and miR-1 level was examined by real-time PCR in vivo and in vitro, respectively. Results: In vivo, AE significantly shortened the QT interval, action potential duration at 90% repolarization (APD90) and resting membrane potential (RMP), which were markedly elongated by HFD. AE increased IK1 current and Kir2.1 protein expression which were reduced in HFD rats. Furthermore, AE significantly inhibited pro-arrhythmic miR-1 in the hearts of HFD rats. In vitro, AE decreased miR-1 expression levels resulting in an increase of Kir2.1 protein levels in cholesterol-enriched NRVMs. Conclusions: AE prevents HFD-induced QT prolongation by repressing miR-1 and upregulating its target Kir2.1. These findings suggest a novel pharmacological role of AE in HFD-induced cardiac electrical remodeling.

scholarly journals Hepatic Lipid Accumulation Induced by a High-fat Diet Is Regulated by Nrf2 Through Multiple Pathways

2021 ◽  
Author(s):  
sheng Qiu ◽  
Zerong Liang ◽  
Qinan Wu ◽  
Miao Wang ◽  
Mengliu Yang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Underlying Mechanism ◽  
Luciferase Assay ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

Abstract BackgroundNuclear factor erythroid 2-related factor 2 (Nrf2) is reportedly involved in hepatic lipid metabolism, but the results are contradictory and the underlying mechanism thus remains unclear. Herein we focused on elucidating the effects of Nrf2 on hepatic adipogenesis and on determining the possible underlying mechanism. We established a metabolic associated fatty liver disease (MAFLD) model in high fat diet (HFD) fed Nrf2 knockout (Nrf2 KO) mice; further, a cell model of lipid accumulation was established using mouse primary hepatocytes (MPHs) treated with free fatty acids (FAs). Using these models, we investigated the relationship between Nrf2 and autophagy and its role in the development of MAFLD.ResultsWe observed that Nrf2 expression levels were up-regulated in patients with MAFLD and diet-induced obese mice. Nrf2 deficiency led to hepatic lipid accumulation in vivo and in vitro, in addition to, promoting lipogenesis mainly by increasing SREBP-1 activity. Moreover, Nrf2 deficiency attenuated autophagic flux and inhibited the fusion of autophagosomes and lysosomes in vivo and in vitro. Weakened autophagy caused reduced lipolysis in the liver. Importantly, Chromatin immunoprecipitation-qPCR (ChIP-qPCR) and dual-luciferase assay results proved that Nrf2 bound to LAMP1 promoter and regulated its transcriptional activity. We accordingly report that Nrf2-LAMP1 interaction has an indispensable role in Nrf2-regulated hepatosteatosis. ConclusionsThese data collectively confirm that Nrf2 deficiency promotes hepatosteatosis by enhancing SREBP-1 activity and attenuating autophagy. To conclude, our data reveal a novel multi-pathway effect of Nrf2 on lipid metabolism in the liver, and we believe that multi-target intervention of Nrf2 signaling is a promising new strategy for the prevention and treatment of MAFLD.

scholarly journals High-Fat Diet Induced Gut Microbiota Alterations Associating With Ghrelin/Jak2/Stat3 Up-Regulation to Promote Benign Prostatic Hyperplasia Development

2021 ◽  
Vol 9 ◽  
Author(s):  
Meng Gu ◽  
Chong Liu ◽  
TianYe Yang ◽  
Ming Zhan ◽  
Zhikang Cai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Benign Prostatic Hyperplasia ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Prostatic Hyperplasia ◽  
Prostate Tissue ◽  
High Fat ◽  
Ghrelin Receptor

The role of high-fat diet (HFD) induced gut microbiota alteration and Ghrelin as well as their correlation in benign prostatic hyperplasia (BPH) were explored in our study. The gut microbiota was analyzed by 16s rRNA sequencing. Ghrelin levels in serum, along with Ghrelin and Ghrelin receptor in prostate tissue of mice and patients with BPH were measured. The effect of Ghrelin on cell proliferation, apoptosis, and induction of BPH in mice was explored. Our results indicated that BPH mice have the highest ratio of Firmicutes and Bacteroidetes induced by HFD, as well as Ghrelin level in serum and prostate tissue was significantly increased compared with control. Elevated Ghrelin content in the serum and prostate tissue of BPH patients was also observed. Ghrelin promotes cell proliferation while inhibiting cell apoptosis of prostate cells. The effect of Ghrelin on enlargement of the prostate was found almost equivalent to that of testosterone propionate (TP) which may be attenuated by Ghrelin receptor antagonist YIL-781. Ghrelin could up-regulate Jak2/pJak2/Stat3/pStat3 expression in vitro and in vivo. Our results suggested that Gut microbiota may associate with Ghrelin which plays an important role in activation of Jak2/Stat3 in BPH development. Gut microbiota and Ghrelin might be pathogenic factors for BPH and could be used as a target for mediation.

The role of 5-HT7 receptors on isoproterenol-induced myocardial infarction in rats with high-fat diet exacerbated coronary endothelial dysfunction

2020 ◽  
Vol 39 (8) ◽  
pp. 1005-1018 ◽  
Author(s):  
I Cinar ◽  
Z Halici ◽  
B Dincer ◽  
B Sirin ◽  
E Cadirci
Keyword(s):  
Myocardial Infarction ◽  
Endothelial Dysfunction ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Heart Tissue ◽  
High Fat ◽  
Inflammatory Status

The presence of 5-HT7r’s in both human and rat cardiovascular and immune tissues and their contribution to inflammatory conditions prompted us to hypothesize that these receptors contribute in acute myocardial infarction (MI) with underlying chronic endothelial dysfunction. We investigated the role of 5-HT7 receptors on heart tissue that damaged by isoproterenol (ISO)-induced MI in rats with high-fat diet (HFD). In vitro and in vivo effects of 5-HT7r agonist (LP44) and antagonist (SB269970) have been investigated on the H9C2 cell line and rats, respectively. For in vivo analyses, rats were fed with HFD for 8 weeks and after this period ISO-induced MI model has been applied to rat. To investigate the role of 5-HT7r’s, two different doses of LP44 and SB269970 were evaluated and compared with standard hypolipidemic agent, atorvastatin. In vitro studies showed that LP44 has protective and proliferative effects on rat cardiomyocytes. Also in in vivo studies stimulating 5-HT7r’s by LP44 improved blood lipid profile (decreased total cholesterol, low-density lipoprotein-C, and triglyceride, increased high-density lipoprotein), decreased cardiac damage markers (creatine kinase and troponin-I), and corrected inflammatory status (tumor necrosis factor-α, interleukin-6). Our results showed significant improvement in LP44 administered rats in terms of histopathologic analyses. In damaged tissues, 5-HT7 mRNA expression increased and agonist administration decreased this elevation significantly. We determined for the first time that 5-HT7r’s are overexpressed in ISO-induced MI of rats with underlying HFD-induced endothelial dysfunction. Restoration of this overexpression by LP44, a 5-HT7r agonist, ameliorated heart tissue in physiopathologic, enzymatic, and molecular level, showing the cardiac role of these receptors and suggesting them as future potential therapeutic targets.

scholarly journals RANKL Is Involved in Runx2-Triggered Hepatic Infiltration of Macrophages in Mice with NAFLD Induced by a High-Fat Diet

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Li Zhong ◽  
Jianghan Yuan ◽  
Lu Huang ◽  
Shan Li ◽  
Liang Deng
Keyword(s):  
High Fat Diet ◽  
Macrophage Infiltration ◽  
Macrophage Migration ◽  
High Fat ◽  
Transwell Assay ◽  
Nonalcoholic Fatty Liver ◽  
Related Transcription Factor

Background. Receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL) is significant in the activation of inflammation. Runt-related transcription factor 2 (Runx2) promotes the hepatic infiltration of macrophages in nonalcoholic fatty liver disease (NAFLD). We studied how RANKL affects Runx2-triggered macrophage infiltration in NAFLD. Method. 30 male C57BL/6J mice at 4 weeks of age were utilized in this study, 20 mice received a high-fat diet (HFD), and 10 mice received standard rodent chow over 8 months. The histopathologic features of the liver were identified by H&E, Oil red O, and Masson staining. Runx2, RANKL, and F4/80 were analyzed by western blot, real-time PCR, and immunohistochemistry in vivo, respectively. Lentivirus or siRNA was utilized for transwell assay to investigate the role of RANKL in Runx2-induced macrophage migration in vitro. Results. Compared to controls, during NAFLD development, HFD increased Runx2 and RANKL in vivo in NASH (P<0.01). Meanwhile, a correlation between the expression of Runx2 and RANKL (P<0.05) was evident. In addition, the hepatic infiltration of macrophages was increased upon HFD feeding, and analysis showed that the macrophage infiltration was correlated with the expression of Runx2 or RANKL (P<0.05). In vitro, we found that overexpression or deficiency of Runx2 increased or decreased the production of RANKL in mHSCs. Then, transwell assay revealed that RANKL was involved in Runx2-induced macrophage migration. Conclusions. Overall, RANKL is involved in Runx2-triggered macrophage migration during NAFLD pathogenesis, which may provide an underlying therapeutic target for NAFLD.

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