scholarly journals The model of rat lipid metabolism disorder induced by chronic stress accompanying high-fat-diet

2011 ◽  
Vol 10 (1) ◽  
pp. 153 ◽  
Author(s):  
Lin Manting ◽  
Zhou Haihong ◽  
Li Jing ◽  
Chen Shaodong ◽  
Liu Yihua
Keyword(s):  
Lipid Metabolism ◽  
Chronic Stress ◽  
High Fat Diet ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder

scholarly journals Metabolomics of the Protective Effect of Ampelopsis grossedentata and Its Major Active Compound Dihydromyricetin on the Liver of High-Fat Diet Hamster

2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Lanlan Fan ◽  
Xiaosheng Qu ◽  
Tao Yi ◽  
Yong Peng ◽  
Manjing Jiang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Protective Effect ◽  
High Fat Diet ◽  
Southern China ◽  
Tricarboxylic Acid Cycle ◽  
Acid Oxidation ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Ampelopsis Grossedentata

The flavonoid dihydromyricetin (DMY) is the main component of Ampelopsis grossedentata (Hand-Mazz) W. T. Wang (AG), a daily beverage and folk medicine used in Southern China to treat jaundice hepatitis, cold fever, and sore throat. Recently, DMY and AG were shown to have a beneficial effect on lipid metabolism disorder. However, the mechanisms of how DMY and AG protect the liver during lipid metabolism disorder remain unclear. In this study, we first analyzed the chemical compounds of AG by HPLC-DAD-ESI-IT-TOF-MSn. Of the 31 compounds detected, 29 were identified based on previous results. Then, the effects of DMY and AG on high-fat diet hamster livers were studied and the metabolite levels and metabolic pathway activity of the liver were explored by 1H NMR metabolomics. Compared to the high-fat diet group, supplementation of AG and DMY attenuated the high-fat-induced increase in body weight, liver lipid deposition, serum triglycerides and total cholesterol levels, and normalized endogenous metabolite concentrations. PCA and PLS-DA score plots demonstrated that while the metabolic profiles of hamsters fed a high-fat diet supplemented with DMY or AG were both far from those of hamsters fed a normal diet or a high-fat diet alone, they were similar to each other. Our data suggest that the underlying mechanism of the protective effect of DMY and AG might be related to an attenuation of the deleterious effect of high-fat diet-induced hyperlipidemia on multiple metabolic pathways including amino acid metabolism, ketone body metabolism, energy metabolism, tricarboxylic acid cycle, and enhanced fatty acid oxidation.

scholarly journals Electroacupuncture Prevents Osteoarthritis of High-Fat Diet-Induced Obese Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Lin-Lin Xie ◽  
Yu-Li Zhao ◽  
Jian Yang ◽  
Hui Cheng ◽  
Zhen-Dong Zhong ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Joint Inflammation ◽  
Protective Effects ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Obese Rats

The effects of acupuncture on osteoarthritis (OA) pathogenesis have been demonstrated in vitro and in animal models. However, the potential for acupuncture to mediate protective effects on obese-induced OA has not been examined. Here, we investigated the effects of different acupuncture patterns on OA pathogenesis in high-fat diet- (HFD-) induced obese rats. After 12-week diet-induced obesity, obese rats were treated with three acupuncture protocols for 2 weeks, including ST36, GB34, and ST36+GB34. The results showed that the three acupuncture protocols both prevented obesity-induced cartilage matrix degradation and MMP expression and mitigated obesity-induced systemic and local inflammation but had different regulatory effects on lipid metabolism and gut microbiota disorder of obese-induced OA rats. Furthermore, the three acupuncture protocols increased the microbial diversity and altered the structure of community of feces in obese rats. We found that ST36 and GB34 could inhibit proinflammatory shift in the gut microbiome with an increase in the ratio of Bacteroidetes/Firmicutes and promote the recovery of relative abundance of Clostridium, Akkermansia, Butyricimonas, and Lactococcus. Although both ST36 and GB34 had an anti-inflammatory effect on serum inflammatory mediators, only the acupuncture protocol with both ST36 and GB34 could effectively inhibit LPS-mediated joint inflammation in obesity rats. Therefore, relieving obesity-related chronic inflammation, lipid metabolism disorder, and gut microbiota disorder may be an important mechanism for acupuncture with ST36 and GB34 to promote OA recovery.

scholarly journals The PCSK9 Involves in the Dyslipidemia of Ovariectomized Mice and Its Mechanism

2021 ◽  
Author(s):  
Dan Zhao ◽  
Xue-qin Zhang ◽  
Wen-jing Guo ◽  
Zhi-hui Cui ◽  
Yi-cheng Wang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
High Fat Diet ◽  
Cholesterol Metabolism ◽  
Critical Role ◽  
Normal Diet ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Pcsk9 Inhibitor ◽  
Metabolism Disorder ◽  
Ovariectomized Mice

Abstract Ovarian failure in postmenopausal female leads E2 to dramatic decrease which is an important reason of menopausal dyslipidemia. PCSK9 as a secretory lipid metabolic regulator plays a critical role in the cholesterol metabolism by negatively regulating LDLR in hepatocytes. Clinical data showed PCSK9 was elevated and positively correlated with LDL-C in the blood of postmenopausal women. However, the relationship between E2 and PCSK9 and the role of PCSK9 in postmenopausal dyslipidemia are still unclear. In this research, 10-week-old ovariectomized mice were fed for 4 weeks with normal diet or high-fat diet, then tested the lipid metabolism profiles and PCSK9 in the blood and the expression of LDLR and PCSK9 in the liver. On this basis, PCSK9-/- ovariectomized mice were used to further verify the effect of PCSK9 in dyslipidemia of ovariectomized mice. Finally, the ovariectomized mice with high-fat diet were subcutaneous injected respectively with E2 or PCSK9 inhibitor alone or both together for 2 weeks and were tested as previous experiment. The results showed PCSK9, TC and LDL-c all increased in the blood of in WT ovariectomized mice and their PCSK9 is positively correlated with LDL-c, while there were on obvious lipid metabolism disorder in the PCSK9−/− ovariectomized mice. PCSK9 inhibitor increased the LDLR on the liver and ameliorated the dyslipidemia in WT ovariectomized mice. It suggests that PCSK9 plays an important role in the dyslipidemia of ovariectomized mice, which provides a new strategy for clinical diagnosis and treatment of the dyslipidemia in post-menopause.

scholarly journals Effect of Tetramethylpyrazine on Atherosclerosis and SCAP/SREBP-1c Signaling Pathway in ApoE−/−Mice Fed with a High-Fat Diet

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Ying Zhang ◽  
Pan Ren ◽  
Qunfu Kang ◽  
Weihong Liu ◽  
Sinai Li ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Signaling Pathway ◽  
High Fat Diet ◽  
Blood Lipids ◽  
Mice Model ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Plaque Area ◽  
Mtorc1 Signaling

Lipid metabolism dysregulation plays a crucial role in the occurrence of atherosclerosis (As). SCAP/SREBP signaling is the main pathway for regulating lipid metabolism. Tetramethylpyrazine (TMP), a Traditional Chinese Medicine (TCM) for treating angina pectoris, has antiatherosclerotic effects and ameliorates blood lipids disturbance. However, its precise mechanism remains unclear. This study investigated the mechanism of TMP in ameliorating As in mice model. After six weeks of high-fat diet, 30 ApoE−/−mice were randomized (n=10) and treated with Lipitor, TMP, or distilled water for six weeks. The serum blood lipids and insulin levels were measured. The expressions of PAQR3, Insig-1, SCAP, SREBP-1c, IRS-1, PI3K, Akt, and mTORC-1 in the adipose tissues were determined. The results showed that TMP could significantly decrease blood lipids levels, insulin, and corrected plaque area of the ApoE−/−mice as compared to the untreated mice (P<0.05,P<0.01). Moreover, TMP could significantly downregulate the expressions of SCAP, SREBP-1c, PAQR3, IRS-1, PI3K, Akt, and mTORC1 (P<0.01). Thus, TMP may ameliorate lipid metabolism disorder and As by downregulating PAQR3 and inhibiting SCAP/SREBP-1c signaling pathway. In addition, PI3K/Akt/mTORC1 signaling pathway may be involved in this process.

scholarly journals Erchen Decoction Ameliorates Lipid Metabolism by the Regulation of the Protein CAV-1 and the Receptors VLDLR, LDLR, ABCA1, and SRB1 in a High-Fat Diet Rat Model

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Shanshan Ding ◽  
Jie Kang ◽  
Ling Tong ◽  
Yuchen Lin ◽  
Linghong Liao ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Visceral Fat ◽  
High Fat Diet ◽  
Positive Control ◽  
Lipid Transport ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Lipid Transporters ◽  
Transport Factors

Lipid metabolism disorder is a common metabolic disorder characterized by abnormal lipid levels in blood. Erchen decoction (ECD) is a traditional Chinese medicine prescription, which is used for the treatment of diseases caused by retention of phlegm dampness. It has been reported to ameliorate the disorder of lipid metabolism. The aim of the present study was to investigate the effects and underlying mechanisms of ECD in lipid metabolism disorder induced by a high-fat diet (HFD) in rats. ECD (4.35g/kg/d) and atorvastatin (10mg/kg/d, positive control) were orally administered to HFD-fed rats for four weeks. The parameters, food, water consumption, body weight, body length, liver, and visceral fat weight and the content of serum lipids and lipid transporters were assessed. The effects of ECD on the mRNA and protein expression levels of lipid transport factors were measured by real-time PCR and western blotting. The present study demonstrated that ECD improved the disorders of serum lipid and lipid transporters in HFD-fed rats, TG (0.70±0.08 mmol/L, p<0.01), LDL-C (1.50±0.19 mmol/L, p<0.01), LDL (1.38±0.21 mmol/L, p<0.05), and oxLDL (1.77±0.39 ng/mL, p<0.05) were downregulated, while HDL-C (0.87±0.13 mmol/L, p<0.01), FFA (0.62±0.13 mmol/L, p<0.05), HDL (38.8±4.0 mg/dL, p<0.05), and CETP (903.6±120.0 ng/mL, p<0.05) were upregulated. But ECD obviously had no effects on the indices food/water/energy intake, body/tissue (liver and fat) weight, and BMI (p>0.05). Concomitantly, ECD reversed the abnormal expressions of those lipid transport factors in the liver and visceral fat.

scholarly journals Rubus Suavissimus Alleviates High-fat Diet-induced Lipid Metabolism Disorder via Modulation of the PPAR / SREBP Pathway in Syrian Golden Hamsters

2020 ◽  
Author(s):  
Man-jing Jiang ◽  
Shuai Huang ◽  
Li Li ◽  
Wan-fang Huang ◽  
Xiao-Sheng Qu ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
High Fat Diet ◽  
Binding Protein ◽  
Diet Group ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Golden Hamsters ◽  
Metabolism Disorder ◽  
Syrian Golden Hamsters

Abstract Background: Rubus suavissimus S. Lee (RS), a sweet plant distributed in southwest of China and used as beverage and folk medicine, has been reported to improve the obesity phenotype and hyperlipidemia. However, the exact molecular mechanism remains unknown.Aim of the study: In this study, we aimed to investigate the preventive effects of RS in lipid metabolism disorder golden hamsters caused by high-fat diet and elucidate the potential molecular mechanisms.Method: Five groups of male LVG Syrian golden hamsters were compared: normal diet group (ND), high-fat diet group (HFD), Xuezhikang Cap group (140 mg/kg; HFD+XZK), low dose of RS group (3.6 g/kg; HFD+RSL), high dose of RS group (7.2 g/kg; HFD+RSH). After eight weeks, biochemical and pathological analyses were conducted to evaluate the preventive effect of RS on lipid metabolism. RT-qPCR, and western blotting analysis were used to explore the potential mechanism underlying.Results: Supplementation of a high-fat diet with RS prevented the symptoms of lipid metabolism disorder of golden hamsters and alleviated liver injury. RS upregulated the expression of the PPAR pathway mediators PPARγ and PPARα as well as its downstream targets CCAAT/enhancer binding protein α (C/EBPα), glucose transporter 4 (Glut4), lipoprotein lipase (LPL), and fatty acid binding protein 4 (aP2). Also, RS downregulated the expression of sterol regulatory element binding protein 1 (SREBP1) and its downstream targets acetyl-CoA carboxylase 1 (ACC1), stearoyl-CoA desaturase-1 (SCD1), and fatty acid synthase (FAS).Conclusions: Our data suggest that RS prevents lipid metabolism disorder golden hamsters in high-fat diet and alleviates liver injury through the regulation of the SREBP/PPAR signaling pathway.

scholarly journals Glucosamine Ameliorates Symptoms of High-Fat Diet-Fed Mice by Reversing Imbalanced Gut Microbiota

2021 ◽  
Vol 12 ◽  
Author(s):  
Xubing Yuan ◽  
Junping Zheng ◽  
Lishi Ren ◽  
Siming Jiao ◽  
Cui Feng ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
Inflammatory Responses ◽  
Fasting Blood Glucose ◽  
Intestinal Barrier ◽  
Intestinal Bacteria ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Rdna Sequencing

Glucosamine (GlcN) is used as a supplement for arthritis and joint pain and has been proved to have effects on inflammation, cancer, and cardiovascular diseases. However, there are limited studies on the regulatory mechanism of GlcN against glucose and lipid metabolism disorder. In this study, we treated high-fat diet (HFD)-induced diabetic mice with GlcN (1 mg/ml, in drinking water) for five months. The results show that GlcN significantly reduced the fasting blood glucose of HFD-fed mice and improved glucose tolerance. The feces of intestinal contents in mice were analyzed using 16s rDNA sequencing. It was indicated that GlcN reversed the imbalanced gut microbiota in HFD-fed mice. Based on the PICRUSt assay, the signaling pathways of glucolipid metabolism and biosynthesis were changed in mice with HFD feeding. By quantitative real-time PCR (qPCR) and hematoxylin and eosin (H&amp;E) staining, it was demonstrated that GlcN not only inhibited the inflammatory responses of colon and white adipose tissues, but also improved the intestinal barrier damage of HFD-fed mice. Finally, the correlation analysis suggests the most significantly changed intestinal bacteria were positively or negatively related to the occurrence of inflammation in the colon and fat tissues of HFD-fed mice. In summary, our studies provide a theoretical basis for the potential application of GlcN to glucolipid metabolism disorder through the regulation of gut microbiota.

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