scholarly journals The modulating effect of ferulic acid on high fat diet induced hyperlipidemia and obesity:A dose response study in male Sprague Dawleyrats

Biomedicine ◽  
2021 ◽  
Vol 41 (2) ◽  
pp. 413-420
Author(s):  
Mumtaz Khan Mohamed ◽  
V. Ramamurthy

Introduction and Aim: Ferulic acid (FA) is a phenolic compound predominantly found in cereals have been used in traditional Chinese medicine. Here, we studied the effect of FA on high-fat diet (HFD) induced hyperlipidemia and obesity in rats.   Materials and Methods:Hyperlipidemia was induced in male Sprague Dawley rats by feeding HFD for 14 weeks. The hypolipidemic effect was evaluated by co-administering 50,100, 200 and 250 mg/kg body weight of FA. At the end of the experimental period, rats were sacrificed and serum/plasma levels of total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), aspartate transaminase (AST), alanine transaminase (ALT), 3-hydroxy-3methyl-glutaryl-coenzyme A reductase (HMG CoA reductase) and adiponectin were determined. Moreover, Histopathological examination of liver and visceral adipose tissue (AT) was also carried out.   Results:HFD treatment significantly increased weight gain, body mass index, total fat pad mass, blood lipids, LDL cholesterol and serum transaminases.HFD +FA fed rats showed a significant decrease in blood lipids and an increase in antioxidant enzymes when compared to the HFD control rats. The activity of HMG CoA reductase and serum adiponectin levels were elevated in rats administered with FA. Among the 4 doses studied, 200 mg of FA/kg body weight exhibited optimum hypolipidemic activity. Histological observations in the liver and visceral AT added additional evidence for the lipid-lowering effect of FA.   Conclusion:These findings indicate that FA can act as a hypolipidemic agent, probably by modulating the activity of HMG CoA reductase and serum adiponectin levels.

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Yi-Hui Liu ◽  
Zhi-Nan Xiang ◽  
Chen Chen ◽  
Luo-Sheng Wan ◽  
Jia-Chun Chen

In this study, C57BL/6J mice with high-fat diet- (HFD-) induced hyperlipidemia were treated with total Liriope spicata var. prolifera polysaccharides (TLSP: 200, 400, and 800 mg/kg body weight), simvastatin (3 mg/kg body weight), or saline for 8 weeks, respectively. The results showed that TLSP had strong lipid-lowering and hepatoprotective effects on C57BL/6J mice with HFD-induced hyperlipidemia. TLSP administration significantly reduced serum total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) levels and downregulated the expressions of peroxisome proliferator-activated receptor (PPAR)γ and fatty acid synthase (FAS) in the adipose and liver tissues of the mice. TLSP exerted hypolipidemic and hepatoprotective effects by activating lipid/bile acid metabolism via the FXH-SHP/CYP7A1 and SEBP-1c/FAC/ACC signaling pathways. Thus, TLPS is a promising natural polymer with hepatoprotective and hypolipidemic properties.


2018 ◽  
Vol 19 (12) ◽  
pp. 3903 ◽  
Author(s):  
Xiaofei Zhu ◽  
Jingyi Yang ◽  
Wenjuan Zhu ◽  
Xiaoxiao Yin ◽  
Beibei Yang ◽  
...  

The natural compound berberine has been reported to exhibit anti-diabetic activity and to improve disordered lipid metabolism. In our previous study, we found that such compounds upregulate expression of sirtuin 1—a key molecule in caloric restriction, it is, therefore, of great interest to examine the lipid-lowering activity of berberine in combination with a sirtuin 1 activator resveratrol. Our results showed that combination of berberine with resveratrol had enhanced hypolipidemic effects in high fat diet-induced mice and was able to decrease the lipid accumulation in adipocytes to a level significantly lower than that in monotherapies. In the high fat diet-induced hyperlipidemic mice, combination of berberine (25 mg/kg/day, oral) with resveratrol (20 mg/kg/day, oral) reduced serum total cholesterol by 27.4% ± 2.2%, and low-density lipoprotein-cholesterol by 31.6% ± 3.2%, which was more effective than that of the resveratrol (8.4% ± 2.3%, 6.6% ± 2.1%) or berberine (10.5% ± 1.95%, 9.8% ± 2.58%) monotherapy (p < 0.05 for both). In 3T3-L1 adipocytes, the treatment of 12 µmol/L or 20 µmol/L berberine combined with 25 µmol/L resveratrol showed a more significant inhibition of lipid accumulation observed by Oil red O stain compared with individual compounds. Moreover, resveratrol could increase the amount of intracellular berberine in hepatic L02 cells. In addition, the combination of berberine with resveratrol significantly increases the low-density-lipoprotein receptor expression in HepG2 cells to a level about one-fold higher in comparison to individual compound. These results implied that the enhanced effect of the combination of berberine with resveratrol on lipid-lowering may be associated with upregulation of low-density-lipoprotein receptor, and could be an effective therapy for hyperlipidemia in some obese-associated disease, such as type II diabetes and metabolic syndrome.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yinhe Cai ◽  
Junmao Wen ◽  
Siwen Ma ◽  
Zhexing Mai ◽  
Qunzhang Zhan ◽  
...  

Macrophage polarization plays a vital impact in triggering atherosclerosis (AS) progression and regression. Huang-Lian-Jie-Du Decoction (HLJDD), a famous traditional Chinese decoction, displays notable anti-inflammatory and lipid-lowering effects in different animal models. However, its effects and mechanisms on AS have not been clearly defined. We determined whether HLJDD attenuated atherosclerosis and plaques vulnerability by regulating macrophage polarization in ApoE−/− mice induced by high-fat diet (HFD). Furthermore, we investigated the effects of HLJDD on macrophage polarization in oxidized low-density lipoprotein (ox-LDL) induced RAW264.7 cells. For in vivo assay, compared with the model group, HLJDD ameliorated lipid metabolism, with significantly decreased levels of serum triglyceride, total cholesterol (CHOL), and lipid density lipoprotein. HLJDD suppressed serum tumor necrosis factor α (TNF-α) and IL-1β levels with increased serum IL-10 level, and inhibited mRNA level of NLRP3 inflammasome in carotid tissues. HLJDD enhanced carotid lesion stability by decreasing macrophage infiltration together with increased expression of collagen fibers and α-SMA. Moreover, HLJDD inhibited M1 macrophage polarization, which decreased the expression and mRNA levels of M1 markers [inducible nitric oxide synthase (iNOS) and CD86]. HLJDD enhanced alternatively activated macrophage (M2) activation, which increased the expression and mRNA levels of M2 markers (Arg-1 and CD163). For in vitro assay, HLJDD inhibited foam cell formation in RAW264.7 macrophages disturbed by ox-LDL. Besides, groups with ox-LDL plus HLJDD drug had a lower expression of CD86 and mRNA levels of iNOS, CD86, and IL-1β, but higher expression of CD163 and mRNA levels of Arg-1, CD163, and IL-10 than ox-LDL group. Collectively, our results revealed that HLJDD alleviated atherosclerosis and promoted plaque stability by suppressing M1 polarization and enhancing M2 polarization.


2018 ◽  
Vol 13 (1) ◽  
pp. 379-384 ◽  
Author(s):  
Xia Qiu ◽  
Wenwen Zhong

AbstractThis study investigated the antihyperglycemic and antihyperlipidemic effects of low-molecular-weight carrageenan (LC) on rats fed a high-fat diet. Wistar rats were divided into five groups: normal control group (NC), high-fat diet control group (HC), carrageenan-treated control group (CC), 1% LC group (1% LC), and 3% LC-groups (3% LC). Body weight, food intake, fecal weight, blood glucose, and serum lipid levels were measured. After 30 days, body weight significantly decreased in the LC-treated groups than in the HC group. Moreover, in the LC-treated groups, postprandial blood glucose, total cholesterol, triglyceride, and low-density lipoprotein cholesterol (LDL-C) levels decreased, whereas high-density lipoprotein cholesterol (HDL-C) levels increased. From this study, our data suggest that LC has antihyperglycemic and hypolipidemic effects when compared to carrageenan, likely related to its increased absorption due to its lower molecular weight.


2012 ◽  
Vol 2 (2) ◽  
pp. 50-60 ◽  
Author(s):  
Kalavarasariel Gopinathanpillai ◽  
Eluri Kalpana ◽  
Balasubramaniam Dineshkumar ◽  
Elumalai Monogaran ◽  
Govindharajalu Geetha ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Débora Maria Soares de Souza ◽  
Guilherme de Paula Costa ◽  
Ana Luísa Junqueira Leite ◽  
Daniela Silva de Oliveira ◽  
Kelerson Mauro de Castro Pinto ◽  
...  

The protozoan Trypanosoma cruzi is responsible for triggering a damage immune response in the host cardiovascular system. This parasite has a high affinity for host lipoproteins and uses the low-density lipoprotein (LDL) receptor for its invasion. Assuming that the presence of LDL cholesterol in tissues could facilitate T. cruzi proliferation, dietary composition may affect the parasite-host relationship. Therefore, the aim of this study was to evaluate myocarditis in T. cruzi-infected C57BL/6 mice—acute phase—fed a high-fat diet and treated with simvastatin, a lipid-lowering medication. Animals (n=10) were infected with 5×103 cells of the VL-10 strain of T. cruzi and treated or untreated daily with 20 mg/kg simvastatin, starting 24 h after infection and fed with a normolipidic or high-fat diet. Also, uninfected mice, treated or not with simvastatin and fed with normolipidic or high-fat diet, were evaluated as control groups. Analyses to measure the production of chemokine (C-C motif) ligand 2 (CCL2), interferon- (IFN-) γ, interleukin- (IL-) 10, and tumor necrosis factor (TNF); total hepatic lipid dosage; cholesterol; and fractions, as well as histopathological analysis, were performed on day 30 using cardiac and fat tissues. Our results showed that the high-fat diet increased (i) parasite replication, (ii) fat accumulation in the liver, (iii) total cholesterol and LDL levels, and (iv) the host inflammatory state through the production of the cytokine TNF. However, simvastatin only reduced the production of CCL2 but not that of other inflammatory mediators or biochemical parameters. Together, our data suggest that the high-fat diet may have worsened the biochemical parameters of the uninfected and T. cruzi-infected animals, as well as favored the survival of circulating parasites.


Author(s):  
Biplav S ◽  
Sindhura G ◽  
Shivalinge Gowda K P

 Objective: The main aim of the present study is concerned with the evaluation of anti-atherosclerotic potential of quercetin in alloxan-induced diabetic rats fed with high-fat diet (HFD).Methods: Atherosclerosis (AS) is the major cause for many of the cardiovascular disease, and it is accelerated in the presence of diabetes mellitus and causes profound alterations in the lipid profile. The method used for the induction of AS was using HFD for 60 days. In this study, rats were divided into four groups (n=6). Group I served as normal control, Group II alloxan (120 mg/kg b.w i.p)-treated diabetic rats, Group III received quercetin (50 mg/ kg b.w p.o), and Group IV received atorvastatin (10 mg/kg b.w p.o) along with alloxan (120 mg/kg b.w i.p) on the 1st day of the days of the study period. AS was induced in Group II, Group III, and Group IV rats by feeding them with HFD from the 1st day to 60th day. The body weight, feed intake was measured daily. The blood was withdrawn from retro-orbital plexus, and the serum was used for the estimation of lipid profile (total cholesterol [TC], triglycerides [TGs], low-density lipoprotein cholesterol [LDL-C], very LDL-C [VLDL-C], and high-density lipoprotein cholesterol [HDL-C]). After scarification under overdose of ketamine, the histopathological study of aorta was carried out.Results: The results showed that the quercetin-treated rats showed a decrease in body weight gain, decreased levels of TC, TGs, LDL-C, and VLDL-C, and increased levels of HDL-C were observed in Group III rats when compared to alloxan-induced diabetic rats fed with HFD (Group III). The histopathological study of aorta showed no development of plaques and of foam cells.Conclusion: From this study, it can be calculated that quercetin has anti-atherosclerotic activity as it significantly altered overall lipid profile in diabetic rats fed with HFD. This activity may be attributed to its antioxidant, inhibition of HMG-CoA reductase activity of quercetin.


2016 ◽  
Vol 5 ◽  
Author(s):  
Haiqiu Huang ◽  
Zhuohong Xie ◽  
Wallace Yokoyama ◽  
Liangli Yu ◽  
Thomas T. Y. Wang

AbstractHypercholesterolaemia is a risk factor for CVD, which is a leading cause of death in industrialised societies. The biosynthetic pathways for cholesterol metabolism are well understood; however, the regulation of circulating cholesterol by diet is still not fully elucidated. The present study aimed to gain more comprehensive understanding of the relationship between circulating cholesterol levels and molecular effects in target tissues using the hamster model. Male golden Syrian hamsters were fed with chow or diets containing 36 % energy from fat with or without 1 % cholesteyramine (CA) as a modulator of circulating cholesterol levels for 35 d. It was revealed that the expression of lanosterol 14α-demethylase (CYP51) instead of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase mRNA expression was responsive to circulating cholesterol in hamsters fed hypercholesterolaemic diets. The high-fat diet increased circulating cholesterol and down-regulated CYP51, but not HMG-CoA reductase. The CA diet decreased cholesterol and increased CYP51 expression, but HMG-CoA reductase expression was not affected. The high-fat diet and CA diet altered the expression level of cholesterol, bile acids and lipid metabolism-associated genes (LDL receptor, cholesterol 7α-hydroxylase (CYP7A1), liver X receptor (LXR) α, and ATP-binding cassette subfamily G member 5/8 (ABCG5/8)) in the liver, which were significantly correlated with circulating cholesterol levels. Correlation analysis also showed that circulating cholesterol levels were regulated by LXR/retinoid X receptor and PPAR pathways in the liver. Using the hamster model, the present study provided additional molecular insights into the influence of circulating cholesterol on hepatic cholesterol metabolism pathways during hypercholesterolaemia.


Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 165
Author(s):  
Aziza Alrafiah

High-fat diet (HFD) is a major problem causing neuronal damage. Thymoquinone (TQ) could regulate oxidative stress and the inflammatory process. Hence, the present study elucidated the significant role of TQ on oxidative stress, inflammation, as well as morphological changes in the cerebellum of rats with HFD. Rats were divided into three groups as (1) control, (2) saturated HFD for eight weeks and (3) HFD supplementation (four weeks) followed by TQ 300 mg/kg/day treated (four weeks). After treatment, blood samples were collected to measure oxidative stress markers glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), and inflammatory cytokines. Furthermore, neuronal morphological changes were also observed in the cerebellum of the rats. HFD rats show higher body weight (286.5 ± 7.4 g) as compared with the control group (224.67 ± 1.78 g). TQ treatment significantly (p < 0.05) lowered the body weight (225.83 ± 13.15 g). TQ produced a significant (p < 0.05) reduction in cholesterol, triglycerides, high-density lipoprotein (HDL), and low-density lipoprotein (LDL). The antioxidative enzymes significantly reduced in HFD rats (GSH, 1.46 ± 0.36 mol/L and SOD, 99.13 ± 5.41 µmol/mL) as compared with the control group (GSH, 6.25 ± 0.36 mol/L and SOD, 159.67 ± 10.67 µmol/mL). MDA was increased significantly in HFD rats (2.05 ± 0.25 nmol/L) compared to the control group (0.695 ± 0.11 nmol/L). Surprisingly, treatment with TQ could improve the level of GSH, MDA, and SOD. TQ treatment significantly (p < 0.05) reduced the inflammatory markers as compared with HFD alone. TQ treatment minimizes neuronal damage as well as reduces inflammation and improves antioxidant enzymes. TQ can be considered as a promising agent in preventing the neuronal morphological changes in the cerebellum of obese populations.


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