Citrus peel extracts attenuated obesity and modulated gut microbiota in mice with high-fat diet-induced obesity

2018 ◽  
Vol 9 (6) ◽  
pp. 3363-3373 ◽  
Author(s):  
Yen-Chen Tung ◽  
Wei-Tien Chang ◽  
Shiming Li ◽  
Jia-Ching Wu ◽  
Vladimir Badmeav ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
High Fat ◽  
Citrus Peel ◽  
Diet Induced Obesity

Polymethoxyflavones (PMFs) and hydroxyl PMFs (HOPMFs) are mainly found in citrus peel and have shown anti-obesity potential in in vitro and in vivo studies.

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.

scholarly journals Obesity, independent of diet, drives lasting effects on intestinal epithelial stem cell proliferation in mice

2018 ◽  
Vol 243 (10) ◽  
pp. 826-835 ◽  
Author(s):  
Weinan Zhou ◽  
Elizabeth A Davis ◽  
Megan J Dailey
Keyword(s):  
High Fat Diet ◽  
Intestinal Epithelial ◽  
Epithelial Stem Cells ◽  
High Fat ◽  
Stem Cell Proliferation ◽  
Epithelial Stem Cell ◽  
Diet Induced Obesity ◽  
And Function

The intestinal epithelium plays an essential role in nutrient absorption, hormone release, and barrier function. Maintenance of the epithelium is driven by continuous cell renewal by intestinal epithelial stem cells located in the intestinal crypts. Obesity affects this process and results in changes in the size and function of the tissue. Because both the amount of food intake and the composition of the diet are contributing factors to developing and maintaining obesity, it is necessary to tease apart the separate contributions of obesity versus the type/amount of diet in driving the epithelial changes. C57BL/6J mice were fed a 60% high-fat diet versus a 10% low-fat diet for three months. A pair fed group was included (mice were fed with high-fat diet, but in equal kcal as that eaten by the low-fat diet- fed mice to keep them lean). We investigated the differences in (1) crypt-villus morphology in vivo, (2) the number and function of differentiated epithelial cell types in vivo, and (3) lasting effects on intestinal epithelial stem cell proliferation and growth in vitro. We found that high-fat diet-induced obesity, independent of the high-fat diet, increased crypt depth, villus height, the number of intestinal epithelial stem cells and goblet cells in vivo, and enhanced the size of the enterospheres developed from isolated IESCs in vitro. In addition, there is an interaction of obesity, type of diet, and availability of the diet (pair fed versus ad libitum) on protein and mRNA expression of alkaline phosphatase (an enzyme of enterocytes). These results suggest that high-fat diet-induced obesity, independent of the high-fat diet, induces lasting effects on intestinal epithelial stem cell proliferation, and drives the differentiation into goblet cells, but an interaction of obesity and diet drives alterations in the function of the enterocytes. Impact statement This study investigates whether obesity or the type/amount of diet differentially alters the proliferation, differentiation, growth, and function of the intestinal epithelial tissue. Although diet-induced obesity is known to alter the growth and function of the epithelium in vivo and cause lasting effects in intestinal epithelial stem cells (IESCs) in vitro, we are the first to tease apart the separate contributions of obesity versus the type/amount of diet in these processes. We found that high-fat diet (HFD)-induced obesity, independent of the HFD, drives lasting effects on IESC proliferation and differentiation into goblet cells, which may contribute to the growth of the epithelium. In addition, there is an interaction of obesity, type of diet, and availability of the diet (PF versus ad libitum) on the function of enterocytes. Identification of the factors driving the epithelial changes may provide new therapeutic strategies to control altered tissue growth and function associated with obesity.

scholarly journals Celastrol inhibits intestinal lipid absorption by reprofiling the gut microbiota to attenuate high-fat diet-induced obesity

iScience ◽  
2021 ◽  
Vol 24 (2) ◽  
pp. 102077
Author(s):  
Hu Hua ◽  
Yue Zhang ◽  
Fei Zhao ◽  
Ke Chen ◽  
Tong Wu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Lipid Absorption ◽  
High Fat ◽  
Diet Induced Obesity

Inhibitory Effects of Fermented Ougan (Citrus reticulata cv. Suavissima) Juice on High-Fat Diet-induced Obesity Associated with White Adipose Tissue Browning and Gut Microbiota Modulation in Mice

2021 ◽  
Author(s):  
Xiao Guo ◽  
Xuedan Cao ◽  
Xiugui Fang ◽  
Ailing Guo ◽  
Erhu Li
Keyword(s):  
Adipose Tissue ◽  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Citrus Reticulata ◽  
Inhibitory Effects ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Tissue Browning

In this study, Ougan juice (OJ) and lactic acid bacteria fermented Ougan juice (FOJ) were investigated individually for their capability of preventing obesity in high-fat diet (HFD)-fed C57BL/6J mice. After...

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.

Seabuckthorn polysaccharide ameliorates high-fat diet-induced obesity by gut microbiota-SCFAs-liver axis

2022 ◽  
Author(s):  
Ying Lan ◽  
Qingyang Sun ◽  
Zhiyuan Ma ◽  
Jing Peng ◽  
Mengqi Zhang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Gut Microbiome ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity

Obesity has been reported to be associated with gut microbiome dysbiosis. seabuckthorn fruits are traditionally used in Tibetan foods and medicines for thousands of years. Seabuckthorn polysaccharide (SP) is one...

Nuciferine improves high-fat diet-induced obesity by reducing intestinal permeability through increasing autophagy and remodeling the gut microbiota

2021 ◽  
Author(s):  
Zhen Shi ◽  
Zhiyuan Fang ◽  
Xinxing Gao ◽  
Hao Yu ◽  
Yiwei Zhu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Intestinal Permeability ◽  
High Fat Diet ◽  
Metabolic Diseases ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Medicinal Value

Nuciferine (NF) has received extensive attention for its medicinal value in the treatment of metabolic diseases, such as obesity, but the effects of NF on obesity-related intestinal permeability, autophagy and...

Black rice anthocyanins alleviate hyperlipidemia, liver steatosis and insulin resistance by regulating lipid metabolism and gut microbiota in obese mice

2021 ◽  
Author(s):  
Haizhao Song ◽  
Xinchun Shen ◽  
Yang Zhou ◽  
Xiaodong Zheng
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Gut Microbiota ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Liver Steatosis ◽  
Obese Mice ◽  
Black Rice ◽  
High Fat ◽  
Diet Induced Obesity

Supplementation of black rice anthocyanins (BRAN) alleviated high fat diet-induced obesity, insulin resistance and hepatic steatosis by improvement of lipid metabolism and modification of the gut microbiota.

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.

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