scholarly journals Consumption of Non-Nutritive Sweetener, Acesulfame Potassium Exacerbates Atherosclerosis through Dysregulation of Lipid Metabolism in ApoE−/− Mice

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3984
Author(s):  
Cheng-Hsin Lin ◽  
Hung-Yuan Li ◽  
Shu-Huei Wang ◽  
Yue-Hwa Chen ◽  
Yang-Ching Chen ◽  
...  

Obesity is associated with the risk of cardiovascular disease, and non-nutritive sweetener, such as acesulfame potassium (AceK) has been used to combat obesity. However, the effects of AceK on cardiovascular disease are still unclear. In this study, high cholesterol diet (HCD)-fed ApoE−/− mice had dysregulated plasma lipid profile, and developed atherosclerosis, determined by atherosclerotic plaque in the aorta. Supplement of AceK in HCD worsened the dyslipidemia and increased atherosclerotic plaque, as compared with HCD-fed ApoE−/− mice. Since treatment of AceK in RAW264.7 macrophages showed no significant effects on inflammatory cytokine expressions, we then investigated the impacts of AceK on lipid metabolism. We found that AceK consumption enhanced hepatic lipogenesis and decreased β-oxidation in ApoE−/− mice. In addition, AceK directly increased lipogenesis and decreased β-oxidation in HepG2 cells. Taken together, a concurrent consumption of AceK exacerbated HCD-induced dyslipidemia and atherosclerotic lesion in ApoE−/− mice, and AceK might increase the risk of atherosclerosis under HCD.

2012 ◽  
Vol 41 (7) ◽  
pp. 957-962 ◽  
Author(s):  
Jun-Hweok Choi ◽  
Hye-Sung Lee ◽  
Young-Eon Kim ◽  
Byoung-Mok Kim ◽  
In-Ho Kim ◽  
...  

2021 ◽  
Author(s):  
Linfeng He ◽  
Cheng Wang ◽  
Yafang Zhang ◽  
Chaocheng Guo ◽  
Yan Wan ◽  
...  

Abstract BackgroundEmodin (EM) is one of bioactive components extracted from Rheum palmatum L. (Dahuang), which possesses numerous pharmacological activities including hypolipidemic effect. However, the potential action of EM on hyperlipidemia (HLP) remains unclear. Here, the theraputic effect of EM against HLP were investigated.MethodsIn this study, the hypolipidemic properties of EM were evaluated using high-cholesterol diet (HCD)-stimulated zebrafish larvae model. The body weight, body length and body mass index (BMI) was measured. The total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) as well as the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected by corresponding assay kits. Tg (flil: eGFP) zebrafish were utilized to observe vascular cholesterol accumulation and Tg (mpx: eGFP) zebrafish to visualize and quantify neutrophil inflammation. The hepatic lipid deposition and hepatic histopathology were analyzed by Oil red O staining and H&E staining, respectively. Finally, the underlying mechanism of EM were investigated using real-time quantitative PCR (RT-qPCR) analysis to assess the gene levels of adenosine monophosphate-activated protein kinase alpha (AMPKα), sterol regulatory element binding protein 2 (SREBP-2), proprotein convertase subtilisin kexin 9 (PCSK9), low-density lipoprotein receptor (LDLR), 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR), adenosine triphosphate binding cassette transporter A1 (ABCA1) and adenosine triphosphate binding cassette transporter G1 (ABCG1).ResultsOur data indicated that EM reduced obesity of zebrafish as evidenced by the decrease in body weight, body length and BMI. EM significantly reduced TC, TG, and LDL-C, and increased HDL-C contents. Moreover, it displayed a prominent inhibitory effect on blood cholesterol accumulation, hepatic lipid accumulation, and neutrophil inflammation in vascular site. Additionally, EM improved the liver function through decreasing ALT and AST levels of zebrafish with HCD-induced hepatosteatosis. Further investigation showed that EM treatment attenuated lipid accumulation via upregulating the expression of AMPKα, LDLR, ABCA1 and ABCG1, and downregulating the expression of SREBP-2, PCSK9 and HMGCR.ConclusionTo conclude, EM alleviated lipid metabolism disorder symptoms caused by HCD via modulating AMPK/SREBP-2/PCSK9/LDLR pathway in larvae, suggesting that EM may be developed into hypolipidmic agent for treating lipid metabolism related diseases.


2009 ◽  
Vol 37 (4) ◽  
pp. 1029-1037 ◽  
Author(s):  
Z Qiao ◽  
J Ren ◽  
H Chen

Lipoprotein-associated phospholipase A2 (Lp-PLA2) contributes to atherosclerotic plaque instability and subsequent sudden coronary death. Statins are associated with decreased stroke risk and may improve stability of atherosclerotic plaques. The present study investigated the effect of simvastatin on expression of Lp-PLA2 levels in atherosclerotic plaques and on Lp-PLA2 activity in atherosclerotic aortas. Rabbits were a fed chow (control group) or a high-cholesterol diet (atherosclerosis group) for 12 weeks. An additional group on the high-cholesterol diet received simvastatin (5 mg/kg per day) for the last 4 weeks (simvastatin group). Lp-PLA2 activity in plasma and atherosclerotic aortas was significantly higher in the atherosclerosis group than in the control group and, consistent with this, abundant Lp-PLA2 protein was detected in plaques in the atherosclerosis group. Simvastatin significantly reduced Lp-PLA2 activity in plasma and aorta tissue, and reduced Lp-PLA2 protein level in atherosclerotic plaques. Whereas there was no significant difference in total atherosclerotic lesion area between simvastatin and atherosclerosis groups, simvastatin significantly reduced macrophage content, lipid retention and the intima/media ratio but increased the content of smooth muscle cells in atherosclerotic lesions. Thus, statin treatment markedly reduced Lp-PLA2 in both plasma and atherosclerotic plaques. This was associated with attenuation of the local inflammatory response and improved plaque stability.


2019 ◽  
Vol 20 (2) ◽  
pp. 76-81
Author(s):  
Jhouharotul Faradisah ◽  
Diah Purwaningsari

Dyslipidemia is an abnormal lipid metabolism which may cause fat degeneration on hepatocytes cells and elevated triglyceride serum level. Dyslipidemia can be prevented by the consumption of high antioxidant food. Noni(Morinda citrifolia) contains many antioxidant such as flavanoid, kuersetin, tannin, and saponin, which are able to prohibit the elevation of ROS.This research is aimed to find out the effect of noni(Morinda citrifolia) extract in reducing the number of hepatocyte’s cells with fat degeneration and decreasing the triglyceride level which is elevated due to high cholesterol diet induction.In this study white rats divided randomly into 4 groups, control group (K-), high cholesterol diet induced group (K+), high cholesterol diet induced with 100 mg/Kg BW noni extract group (P1), high cholesterol diet induced with 200 mg/Kg BW noni extract group (P2). The result shows that noni  extract with dose 100 mg/Kg BW and  200 mg/Kg BWcan reduce the number of hepatocytes cells with fat degeneration (p= 0,026 and p=0,027) and decrease the level of triglyceride serum (p=0,036 and p=0,010).The conclusion is noni extract with dose 100 mg/KgBW reduces effectively  the number of hepatocyte’s cells with fat degeneration and decreases the level of triglyceride serum which increase because of high cholesterol diet. 


1979 ◽  
Vol 42 (2) ◽  
pp. 209-216 ◽  
Author(s):  
D. G. Oakenfull ◽  
Dorothy E. Fenwick ◽  
R. L. Hood ◽  
D. L. Topping ◽  
R. L. Illman ◽  
...  

1. The effects of feeding isolated saponins on plasma lipid concentrations and on concentrations of biliary and faecal bile acids and neutral sterols were studied in the rat.2. The animals were given one of four diets, i.e. a standard low-cholesterol synthetic diet, the diet+10 g saponins/kg, the diet+10 g cholesterol/kg, the diet+10 g cholesterol+10 g saponins/kg.3. Saponins partially reversed the hypercholesterolaemia caused by the high-cholesterol diet and increased both the rate of bile acid secretion and the faecal excretion of bile acids and neutral sterols. The proportionate contribution of the primary bile acids (particularly chenodeoxycholic) to faecal excretion was also increased by saponins.4. The results are discussed in relation to the hypothesis that saponins act by inducing the adsorption of bile acids by dietary fibre.


2013 ◽  
Vol 12 (1) ◽  
pp. 67 ◽  
Author(s):  
Xu Hu ◽  
Tao Wang ◽  
Wei Li ◽  
Feng Jin ◽  
Li Wang

2020 ◽  
pp. 1-8
Author(s):  
Christian Caceres ◽  
Mi-Bo Kim ◽  
Minkyung Bae ◽  
Tho X. Pham ◽  
Yoojin Lee ◽  
...  

Abstract Lipid metabolism and inflammation contribute to CVD development. This study investigated whether the consumption of cranberries (CR; Vaccinium macrocarpon) can alter HDL metabolism and prevent inflammation in mice expressing human apo A-I transgene (hApoAITg), which have similar HDL profiles to those of humans. Male hApoAITg mice were fed a modified American Institute of Nutrition-93M high-fat/high-cholesterol diet (16 % fat, 0·25 % cholesterol, w/w; n 15) or the high-fat/high-cholesterol diet containing CR (5 % dried CR powder, w/w, n 16) for 8 weeks. There were no significant differences in body weight between the groups. Serum total cholesterol, non-HDL-cholesterol and TAG concentrations were significantly lower in the control than CR group with no significant differences in serum HDL-cholesterol and apoA-I. Mice fed CR showed significantly lower serum lecithin–cholesterol acyltransferase activity than the control. Liver weight and steatosis were not significantly different between the groups, but hepatic expression of genes involved in cholesterol metabolism was significantly lower in the CR group. In the epididymal white adipose tissue (eWAT), the CR group showed higher weights with decreased expression of genes for lipogenesis and fatty acid oxidation. The mRNA abundance of F4/80, a macrophage marker and the numbers of crown-like structures were less in the CR group. In the soleus muscle, the CR group also demonstrated higher expression of genes for fatty acid β-oxidation and mitochondrial biogenesis than those of the control. In conclusion, although CR consumption elicited minor effects on HDL metabolism, it prevented obesity-induced inflammation in eWAT with concomitant alterations in soleus muscle energy metabolism.


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