Choline and methionine regulate lipid metabolism via the AMPK signaling pathway in hepatocytes exposed to high concentrations of nonesterified fatty acids

2019 ◽  
Vol 121 (8-9) ◽  
pp. 3667-3678 ◽  
Author(s):  
Jing Shen ◽  
Bofei Sun ◽  
Chao Yu ◽  
Yangchun Cao ◽  
Chuanjiang Cai ◽  
...  
Author(s):  
Hui Chen ◽  
Liang Zhang ◽  
Xinwei Li ◽  
Xiaobing Li ◽  
Guoquan Sun ◽  
...  

2020 ◽  
Vol 99 (1) ◽  
pp. 224-234
Author(s):  
Chunyan Fu ◽  
Yan Zhang ◽  
Qimeng Yao ◽  
Xiangfa Wei ◽  
Tianhong Shi ◽  
...  

1990 ◽  
Vol 36 (12) ◽  
pp. 2109-2113 ◽  
Author(s):  
R Siekmeier ◽  
W März ◽  
W Gross

Abstract Recently, polyanion precipitation assays for low-density lipoprotein (LDL)-cholesterol have been found to underestimate their analyte in normolipidemic samples (Siekmeier et al., Clin Chim Acta 1988;177:221-30). Therefore, accuracy, specificity, and interference by nonesterified fatty acids have been studied for three precipitants (obtained by heparin, dextran sulfate, or polyvinyl sulfate precipitation). At normal concentrations of LDL, precipitation is incomplete, whereas it is nearly quantitative at high concentrations of LDL. The polyvinyl sulfate reagent markedly responds to variations in the amount of non-LDL protein present in the precipitation mixture. In the dextran sulfate and the polyvinyl sulfate method, but not in the heparin method, the percentages of LDL precipitated notably increase as the concentration of the polyanion compound is decreased. In either assay, very-low-density lipoproteins, but not high-density lipoproteins, are significantly coprecipitated (dextran sulfate 28%, polyvinyl sulfate and heparin 66%) in a concentration-independent fashion. Increased concentrations of nonesterified fatty acids markedly interfere with the dextran sulfate and polyvinyl sulfate assay, but do not much affect results with the heparin reagent.


2015 ◽  
Vol 116 (6) ◽  
pp. 1070-1079 ◽  
Author(s):  
Qinghua Deng ◽  
Guowen Liu ◽  
Lei Liu ◽  
Yuming Zhang ◽  
Liheng Yin ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Mi-Rae Shin ◽  
Min Ju Kim ◽  
Hae-Jin Park ◽  
Jegeun Han ◽  
Seong-Soo Roh

Objective. Liver kinase B (LKB) 1 and AMP-activated protein kinase (AMPK) are master regulators and sensors for energy homeostasis. AMPK is mainly activated via phosphorylation of LKB1 under energy stress. Here, we highlighted the antiobesity effect and underlying mechanism of Taraxacum coreanum Nakai (TCN) in connection with LKB1-AMPK signaling pathway. Methods. Male C57BL/6 mice were fed on a high-fat diet (60% kcal fat; HFD) to induce obesity. Simultaneously, they received 100 or 200 mg/kg TCN orally for 5 weeks. We measured the body weight gain and liver weight along with liver histology. Moreover, the changes of factors related to lipid metabolism and β-oxidation were analyzed in the liver, together with blood parameters. Results. The body weights were decreased in mice of the TCN200 group more than those of the HFD control group. Moreover, TCN supplementation lowered serum triglyceride (TG) and total cholesterol (TC) levels, whereas TCN increased HDL-cholesterol level. Liver pathological damage induced by HFD was alleviated with TCN treatment and accompanied with significant reduction in serum AST and ALT activities. In addition, TCN significantly increased the expression of p-AMPK compared with the HFD control group via the activation of LKB1/AMPK signaling pathway. Lipid synthesis gene like ACC was downregulated and factors related to β-oxidation such as carnitine palmitoyl transferase-1 (CPT-1) and uncoupling protein 2 (UCP-2) were upregulated through peroxisome proliferator-activated receptor (PPAR) α activation. Conclusion. Taken together, these data suggest that TCN treatment regulates lipid metabolism via LKB1-AMPK signaling pathway and promotes β-oxidation by PPARα; hence, TCN may have potential remedy in the prevention and treatment of obesity.


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