scholarly journals High-Fat Diets-Induced Metabolic Disorders to Study Molecular Mechanism of Hyperlipidemia in Rats

2021 ◽  
Vol 3 (2) ◽  
pp. 38-50
Author(s):  
Harfi Maulana ◽  
Ahmad Ridwan
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Cholesterol Homeostasis ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Signaling Mechanism ◽  
Signaling Systems ◽  
Metabolism Disorder ◽  
Lipid Metabolism Disorders ◽  
Primary Literature

Hyperlipidemia is a lipid metabolism disorder occurring due to consumption of a high-fat diet (HFD), which contributes to atherosclerosis and cardiovascular disease development. HFD causes metabolic problems in Rodentia animals like human metabolic abnormalities, making it a popular model for studying the signaling systems involved. Hyperlipidemia is a condition in which the body's cholesterol levels elevate. In recent years, several studies have investigated the relationship between HFD feeding and hyperlipidemia and signaling pathways involved in cholesterol homeostasis. However, this signaling mechanism in lipid metabolism has not been fully explained, so additional analysis is needed. The present study aimed to investigate the mechanism that occurs from hyperlipidemia due to HFD feeding. The method used is a literature review approach following the PRISMA scheme for selecting the primary literature, including identification, screening, eligibility test, and inclusion. Eleven articles included primary literature with credibility (H-index) of 20, 33, 71, 92, 93, 162, 180, 192, and 332 (six articles from Q1 journals and five from Q2 journals). Long-term administration of HFD directly affects lipid metabolism, including an increase in the concentration of total cholesterol, triglycerides, LDL, and a decrease in HDL concentration, followed by an increase in body weight. In addition, HFD also disrupts adipose tissue and insulin resistance. The conclusion of this study is that HFD can cause hyperlipidemia either directly or indirectly by inducing insulin resistance, which contributes to lipid metabolism disorders.  

Chlorpyrifos exposure induces lipid metabolism disorder at the physiological and transcriptomic levels in larval zebrafish

2019 ◽  
Vol 51 (9) ◽  
pp. 890-899
Author(s):  
Xiaoyu Wang ◽  
Jiajie Zhou ◽  
Manlu Shen ◽  
Jiayan Shen ◽  
Xinyue Zhang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Acid Synthesis ◽  
Treated Group ◽  
Heart Tissue ◽  
Lipid Metabolism Disorder ◽  
Larval Zebrafish ◽  
Metabolism Disorder ◽  
Glucose And Lipid Metabolism ◽  
Lipid Metabolism Disorders ◽  
Cellular Apoptosis

Abstract Chlorpyrifos (CPF) is a widely used insecticide in pest control, and it can affect aquatic animals by contaminating the water. In this study, larval zebrafish were exposed to CPF at concentrations of 30, 100 and 300 μg/l for 7 days. In the CPF-treated group, lipid droplet accumulation was reduced in larval zebrafish. The levels of triglyceride (TG), total cholesterol (TC), and pyruvate were also decreased after CPF exposure. Cellular apoptosis were significantly increased in the heart tissue after CPF exposure compared with the control. Transcription changes in cardiovascular genes were also observed. Through transcriptome analysis, we found that the transcription of 465 genes changed significantly, with 398 upregulated and 67 downregulated in the CPF-treated group, indicating that CPF exposure altered the transcription of genes. Among these altered genes, a number of genes were closely related to the glucose and lipid metabolism pathways. Furthermore, we also confirmed that the transcription of genes related to fatty acid synthesis, TC synthesis, and lipogenesis were significantly decreased in larval zebrafish after exposure to CPF. These results indicated that CPF exposure induced lipid metabolism disorders associated with cardiovascular toxicity in larval zebrafish.

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 Tangduqing Granules Attenuate Insulin Resistance and Abnormal Lipid Metabolism through the Coordinated Regulation of PPARγ and DGAT2 in Type 2 Diabetic Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Qinghua Zhang ◽  
Yingying Huang ◽  
Xiaojin Li ◽  
Hongyi Liu ◽  
Baichuan He ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Lipid Metabolism ◽  
Insulin Sensitivity ◽  
Fasting Blood Glucose ◽  
Diabetic Rat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder ◽  
Type 2 Diabetic

Insulin resistance (IR) is a vital hallmark of type 2 diabetes mellitus, which is characterized by an impaired ability of insulin to promote glucose uptake and utilization. Lipid deposition is closely associated with impaired insulin sensitivity. PPARγ plays an important role in glucose homeostasis, adipocyte differentiation, and insulin sensitivity. Likewise, DGAT2 also exerts a crucial role in integrating carbohydrate and lipid metabolism in the liver. The present study is aimed at evaluating a Chinese medicinal formula, Tangduqing granules (TDQ), with multifaceted actions against lipid and glucose metabolism disorder and IR of type 2 diabetes. An animal model of type 2 diabetes was developed by high-fat diet feeding plus low-dose streptozotocin injection. After oral administration of TDQ for 5 weeks, the effects on glucose and lipid metabolism and the underlying mechanism were evaluated by biochemical, histological, RT-PCR, and western blotting methods. The results showed that TDQ decreased fasting blood glucose, ameliorated glucose tolerance, and improved IR. Besides, TDQ regulated hyperlipidemia symptoms, decreased serum lipid levels and liver TG, and reduced hepatic steatosis in a type 2 diabetic rat model. Furthermore, TDQ reversed diabetes-induced decrease in the mRNA and protein expression of PPARγ and elevation in the mRNA and protein levels of DGAT2 in the liver. In addition, we showed that interference of TDQ ameliorated palmitate-induced glucose and lipid metabolic abnormalities in HepG2 cells. TDQ are, therefore, a potential Chinese medicinal formula that relieves IR and lipid metabolism disorder might be through promotion of PPARγ and decrease of DGAT2 expression.

scholarly journals Electroacupuncture Mitigates Skeletal Muscular Lipid Metabolism Disorder Related to High-Fat-Diet Induced Insulin Resistance through the AMPK/ACC Signaling Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Zhixing Li ◽  
Danchun Lan ◽  
Haihua Zhang ◽  
Hongtao Zhang ◽  
Xiaozhuan Chen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
High Fat Diet ◽  
Control Group ◽  
Sensitivity Index ◽  
Model Assessment ◽  
Sprague Dawley ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Metabolism Disorder

The aim of this work is to investigate the effect of electroacupuncture (EA) on insulin sensitivity in high-fat diet (HFD) induced insulin resistance (IR) rats and to evaluate expression of AMPK/ACC signaling components. Thirty-two male Sprague-Dawley rats were randomized into control group, HFD group, HFD+Pi (oral gavage of pioglitazone) group, and HFD+EA group. Acupuncture was subcutaneously applied to Zusanli (ST40) and Sanyinjiao (SP6). For Zusanli (ST40) and Sanyinjiao (SP6), needles were connected to an electroacupuncture (EA) apparatus. Fasting plasma glucose was measured by glucose oxidase method. Plasma fasting insulin (FINS) and adiponectin (ADP) were determined by ELISA. Triglyceride (TG) and cholesterol (TC) were determined by Gpo-pap. Proteins of adiponectin receptor 1 (adipoR1), AMP-activated Protein Kinase (AMPK), and acetyl-CoA carboxylase (ACC) were determined by Western blot, respectively. Compared with the control group, HFD group exhibits increased levels of FPG, FINS, and homeostatic model assessment of insulin resistance (HOMA-IR) and decreased level of ADP and insulin sensitivity index (ISI). These changes were reversed by both EA and pioglitazone. Proteins of adipoR1 and AMPK were decreased, while ACC were increased in HFD group compared to control group. Proteins of these molecules were restored back to normal levels upon EA and pioglitazone. EA can improve the insulin sensitivity of insulin resistance rats; the positive regulation of the AMPK/ACC pathway in the skeletal muscle may be a possible mechanism of EA in the treatment of IR.

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.

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