lipid metabolism disorder
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2022 ◽  
Vol 12 ◽  
Author(s):  
Xiao Qi Liu ◽  
Ting Ting Jiang ◽  
Meng Ying Wang ◽  
Wen Tao Liu ◽  
Yang Huang ◽  
...  

BackgroundLipid metabolism disorder, as one major complication in patients with chronic kidney disease (CKD), is tied to an increased risk for cardiovascular disease (CVD). Traditional lipid-lowering statins have been found to have limited benefit for the final CVD outcome of CKD patients. Therefore, the purpose of this study was to investigate the effect of microinflammation on CVD in statin-treated CKD patients.MethodsWe retrospectively analysed statin-treated CKD patients from January 2013 to September 2020. Machine learning algorithms were employed to develop models of low-density lipoprotein (LDL) levels and CVD indices. A fivefold cross-validation method was employed against the problem of overfitting. The accuracy and area under the receiver operating characteristic (ROC) curve (AUC) were acquired for evaluation. The Gini impurity index of the predictors for the random forest (RF) model was ranked to perform an analysis of importance.ResultsThe RF algorithm performed best for both the LDL and CVD models, with accuracies of 82.27% and 74.15%, respectively, and is therefore the most suitable method for clinical data processing. The Gini impurity ranking of the LDL model revealed that hypersensitive C-reactive protein (hs-CRP) was highly relevant, whereas statin use and sex had the least important effects on the outcomes of both the LDL and CVD models. hs-CRP was the strongest predictor of CVD events.ConclusionMicroinflammation is closely associated with potential CVD events in CKD patients, suggesting that therapeutic strategies against microinflammation should be implemented to prevent CVD events in CKD patients treated by statin.


2022 ◽  
Vol 88 ◽  
pp. 104901
Author(s):  
Dandan Wang ◽  
Zequn Yin ◽  
Lan Han ◽  
Mengxue Zhang ◽  
Huaxin Li ◽  
...  

Author(s):  
Yuanyang Li ◽  
Leiqi Zhu ◽  
Chong Guo ◽  
Mengzhen Xue ◽  
Fangqi Xia ◽  
...  

Abstract: Lipid metabolism disorder is a multifactor issue, which contributes to several serious health consequences, such as obesity, hyperlipidemia, atherosclerosis diabetes, non-alcoholic fatty liver etc. Tannins, applied as natural derived plant, are commonly used in the study of lipid metabolism disease with excellent safety and effectiveness, while producing less toxic and side effects. Meanwhile, recognition of the significance of dietary tannins in lipid metabolism disease prevention has increased. As suggested by existing evidence, dietary tannins can reduce lipid accumulation, block adipocyte differentiation, enhance antioxidant capacity, increase the content of short-chain fatty acids, and lower blood lipid levels, thus alleviating lipid metabolism disorder. This study is purposed to sum up and analyze plenty of documents on tannins, so as to provide the information required to assess the lipid metabolism of tannins.


Author(s):  
Sen Zhang ◽  
Fenfang Hong ◽  
Chen Ma ◽  
Shulong Yang

: Lipid metabolism disorder plays a fundamental role in the pathogenesis of atherosclerosis. As the largest metabolic organ of the human body, liver has a key role in lipid metabolism by influencing fat production, fat decomposition, and the intake and secretion of serum lipoproteins. Numerous clinical and experimental studies have indicated that the dysfunction of hepatic lipid metabolism is closely tied to the onset of atherosclerosis. However, the identity and functional role of hepatic lipid metabolism responsible for these associations remain unknown. This review presented that cholesterol synthesis, cholesterol transport, and the metabolism of triglyceride, lipoproteins, and fatty acids are all associated with hepatic lipid metabolism and atherosclerosis. Moreover, we also discussed the roles of gut microbiota, inflammatory response, and oxidative stress in the pathological association between hepatic lipid metabolism and atherosclerosis. These significant evidences support strongly that hepatic lipid metabolism disorders may increase the risk of atherosclerosis.


2021 ◽  
Author(s):  
Ying Zhang ◽  
Xinyun Dun ◽  
Benying Li ◽  
Hongxu Bao ◽  
Danchuan Li ◽  
...  

Abstract Background: PM exposure can lead to myocardial hypertrophy, with a potential contribution via DNA methylation. Myocardial lipotoxicity is closely related to myocardial hypertrophy. But, myocardial lipotoxicity caused by PM has not been reported. PDGFRβ, a platelet-derived growth factor receptor, is also essential for normal cardiovascular development. However, It is unclear the role of PM-induced PDGFRβ methylation in myocardial hypertrophy and myocardial lipotoxicity. We investigated the effect of PDGFRβ methylation induced by PM on myocardial hypertrophy and myocardial lipotoxicity. Results: PDGFRβ methylation caused by PM decreased PDGFRβ mRNA and protein expression in C57BL/6J mouse hearts. Thus inhibiting gene expression in its downstream pathway, ultimately leading to cardiac hypertrophy. Disturbances of myocardial lipid metabolism caused by PM in AC16 cells and C57BL/6J mouse hearts were also observed. High expression of PDGFRβ in neonatal rat primary cardiomyocytes was found to activate its downstream pathway and ameliorate the effects of PM-induced cardiac hypertrophic activity. At the same time, adenovirus was used to induce high expression of PDGFRβ in C57BL/6J mice. It was found that PDGFRβ not only improved PM-induced cardiac hypertrophy, but also alleviated PM-induced myocardial lipotoxicity. Conclusions: PDGFRβ gene methylation may be one of the potential biomarkers of myocardial hypertrophy induced by PM exposure. And high expression of PDGFRβ may be a potential way to prevent myocardial hypertrophy and cardiac lipid metabolism disorder caused by PM exposure in mice.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jian Li ◽  
Jing Qi ◽  
Yishu Tang ◽  
Huaizheng Liu ◽  
Kefu Zhou ◽  
...  

AbstractOur study aimed to explore the function of circRNA_0001805 in the pathogenesis of NAFLD and the underlying mechanism. A nanodrug system (GA-RM/GZ/PL) was constructed to overexpress circRNA_0001805 specifically in hepatocytes for the treatment of NAFLD. Fat droplet accumulation in cultured cells and mouse hepatic tissues was detected using Oil Red O or H&E staining. The relative expression of circRNAs, genes associated with lipogenesis was quantified by qRT-PCR. Interactions between circRNA_0001805 and miR-106a-5p/miR-320a, between miR-106a-5p/miR-320a and ABCA1/CPT1 were confirmed by dual-luciferase reporter assay. A novel metalorganic framework nanocarrier (GZ) was prepared from glycyrrhizic acid and zinc ions (Zn2+), and this nanocarrier was loaded with the circRNA_0001805 plasmid to construct a nanocore (GZ/PL). Then, this GZ/PL was coated with a galactose-modified RBC membrane (GA-RM) to generate GA-RM/GZ/PL. CircRNA_0001805 expression was downregulated in FFA-challenged primary hepatocytes, HFD-fed mice and NAFLD patients. Overexpressed circRNA_0001805 attenuated NAFLD development by suppressing lipid metabolism disorder and inflammation. CircRNA_0001805 targeted miR-106a-5p/miR-320a, which served as an upstream inhibitor of ABCA1/CPT1 and collaboratively regulated NAFLD progression. GA-RM/GZ/PL targeted hepatocytes, overexpressed circRNA_0001805, released glycyrrhizic acid to reduce the accumulation of lipids in the liver and played a synergistic role against NAFLD-induced lipid metabolism disorder. Graphical Abstract


2021 ◽  
Vol 12 ◽  
Author(s):  
Qiulin Yue ◽  
Zhongjian Wang ◽  
Xueyang Tang ◽  
Chen Zhao ◽  
Kunlun Li ◽  
...  

The fermentation of food materials with suitable probiotic strains is an effective way to improve biological activities. In this study, seaweed extracts were fermented by Saccharomyces cerevisiae and Lactiplantibacillus plantarum, and the hypolipidemic effects of the fermentation products were investigated. In vitro experiments suggested that fermented seaweed extracts have a high capacity for bile acid-binding. Additionally, a significant inhibitory effect against pancreatic lipase was observed. Furthermore, effects in hyperlipidemic mice were determined. Fermented seaweed extracts can alleviate lipid metabolism disorder. The administration of fermented seaweed extracts to mice showed decreased total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) levels and increased high-density lipoprotein cholesterol (HDL-C) levels. Combined, these results suggest that fermented seaweed extracts perform a potent hypolipidemic action, thus providing an effective method for the preparation of functional foods to combat cardiovascular diseases.


Author(s):  
Harfi Maulana ◽  
Ahmad Ridwan

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.  


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