目的：探讨尿毒症维持性血透(MHD)患者营养不良、炎症与脂质代谢紊乱三者间的相关关系，以及对心血管并发症的预测。方法:测51例尿毒症维持性血透患者血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)、载脂蛋白(Apo)A1、ApoB、脂蛋白（a）LP(a)、白蛋白(ALB)、C反应蛋白(CRP)、血清铁蛋白（SF），与30例正常人进行对照研究。结果：MHD患者TG、LDL、ApoB、LP(a)、CRP、SF显著增高,HDL、ApoA1、ALB显著降低(P＜0.05)；随着透析时间的延长，各项检测指标变化进一步加重；且心血管事件发生者血清CRP和LP(a)明显增高，ALB明显降低，血脂紊乱更显著。相关性分析：ALB与HDL、ApoA1正相关，与CRP、LP(a)、TC、TG、ApoB负相关；CRP与LP(a)、TC、TG、ApoB、LDL、SF正相关，与HDL、ApoA1负相关，P均＜0.05。结论：MHD患者存在明显的脂质代谢紊乱、炎症和营养不良，三者的相互促进和影响可能是心血管事件发生的危险因素。
Calcific aortic valve disease has been the most common heart valve disorder in western world, accompanying with the increase of morbidity in our country year by year. Several molecules and mechanisms are involved in the progression of aortic valve calcification, which intensify the complexity of this pathological process. It is known that inflammation, a key factor in many diseases, has its own role in the development of aortic valve calcification. It has been demonstrated that inflammation, one of the most important participants in this disorder, which may accelerate the local lesions in aortic valve via promoting the expression of osteogenic differentiation of associated factors or decreasing the level of protective molecules. Dyslipidemia is a traditional risk factor of cardiovascular events. However, it may induce or enhance the inflammatory response whereby facilitates the calcific lesions in aortic valve. Recently, several researches have illustrated that non-coding RNAs, a stimulative factor in the progression of malignant tumor, might play a role in the development of aortic valve calcification. MiRNA and lncRNA, the non-coding RNAs which regulate the expression of genes involved in inflammatory and osteogenic differentiation, are undeniable regulators of aortic valve calcification.
ObjectiveTo study the effects of ATP citrate lyase (ACLY) gene on proliferation, apoptosis, invasion, and lipid metabolism of colon cancer cells.MethodsColon cancer cells HCT116 were transfected with lentiviral knockdown ACLY gene in vitro and divided into three groups according to cell treatment: HCT116 cells with ACLY gene knockdown as knockdown group, empty vector transfected cells as negative control group, and untreated colon cancer HCT116 cells as blank control group. After the stable new cell line was screened with puromycin, the expression of ACLY protein was detected by Western blot method, the lipid production of cells was detected by triglyceride test kit, the proliferation ability of cells was detected by CCK-8 method, the apoptosis rate was detected by flow cytometry, and the migration ability of cells was detected by cell scratch test.ResultsThe cell survival rate of the knockdown group was lower than those of the blank control group and the negative control group at 120 h, but there was no significant difference among the three groups at 24 h and 48 h. Compared with the negative control group and the blank control group, the apoptosis rate in the knockdown group increased, the 24 h migration ability and the level of intracellular triglyceride decreased.ConclusionACLY gene knockdown can inhibit the proliferation, apoptosis, and migration of colon cancer cells, and its mechanism may be related to the decrease of lipid synthesis ability of colon cancer cells.
Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes, and it is the main cause of vision loss in diabetic patients. Angiopoietin (Ang), a superfamily of secreted proteins, is a vascular growth factor that regulates the stability of vascular environment, participates in angiogenesis and repair, and lipid metabolism. It plays an important role in the development of DR and has become a new target for the treatment of diabetic retinopathy. With the in-depth study of Ang and the research and development of various drugs for Ang, it is expected to bring new ideas and strategies for the treatment of DR in the future.
ObjectiveTo explore the metabolic changes during the differentiation of 3T3-L1 adipocytes caused by the treatment of the transient receptor potential vanilloid 4 (TRPV4)-specific agonist GSK1016790A basing on ultra-performance liquid chromatography-mass spectrometry technology. MethodsMouse 3T3-L1 cells were treated with GSK1016790A at different concentrations (0.1, 1, and 10 μmol/L), and the effect of drugs on cell proliferation was detected by cell counting kit-8 method. A mature adipocyte model was constructed, and GSK1016790A was used to activate TRPV4 channel protein activity and verify the expression levels of TRPV4 and triglycerides. Cell metabolites were collected for metabolomic studies, differential metabolites were screened between groups, and related metabolic pathways were analyzed. Results After GSK1016790A intervened in mature adipocytes, the expression levels of TRPV4 mRNA and triglycerides in cells were significantly upregulated (P<0.05). Metabolomics detection found that GSK1016790A screened a total of 45 differential metabolites such as 2-amino-1,3,4-octadecanetriol, linoleic acid, sphingosine, sphinganine, sn-glycerol-3-phosphate and uridine, mainly involving 13 possible metabolic pathways such as sphingolipid metabolism and biosynthesis of unsaturated fatty acids. Conclusion GSK1016790A may promote adipogenesis in adipocytes by activating TRPV4 channel protein activity, and at the same time participate in regulating metabolic pathways such as the biosynthesis of unsaturated fatty acids pathway and sphingolipid metabolism pathway, affecting lipid metabolism in adipocytes.
ObjectiveTo investigate the association of lipid metabolism and other markers with microvascular invasion in hepatocellular carcinoma (HCC) and to develop a preoperative prediction model from it. MethodsData from 389 HCC patients who underwent hepatectomy at First Hospital of Lanzhou University between January 2017 and March 2023 were retrospectively analyzed. These patients were divided into training group (n=272) and validation group (n=117) with a ratio of 7 : 3. The independent risk factors of microvascular invasion (MVI) were determined by univariate and multivariate logistic regression analysis, and the MVI prediction model was established. The prediction efficiency of the model was verified by the analysis of calibration curve, receiver operating characteristic (ROC) curve and decision curve. ResultsUnivariate and multivariate logistic regression analysis showed that the risk factors independently related to MVI before operation included total cholesterol, lactate dehydrogenase, body mass index, alpha-fetoprotein, carbohydrate antigen 125, hepatitis B DNA, maximum tumor diameter and albumin-bilirubin score. MVI prediction model was established based on the above eight risk factors, and its area under ROC curve in the training group and the validation group were 0.79 [95%CI (0.74, 0.84)] and 0.75 [95%CI (0.66, 0.84)] respectively. Calibration curve analysis showed that the prediction curve fitted well with the standard curve. ROC curve analysis showed that the MVI prediction model was efficient. Decision curve analysis confirmed that the MVI prediction model had significant clinical applications. ConclusionThis study identified independent correlations between total cholesterol levels, among other things, and MVI, and successfully developed and validated novel predictive model based on these indicators that can help physicians effectively identify individuals at high risk for MVI in patients with hepatocellular carcinoma preoperatively, leading to more rational treatment choices.
The poor treatment effect and short survival period of patients with acute leukemia are mainly due to the lack of effective early diagnosis and treatment targets. Lipid metabolism reprogramming meets the material and energy requirements for rapid proliferation and division of tumor cells, and is associated with the invasiveness, recurrence, and chemotherapy resistance of acute leukemia. This article reviews the carcinogenic and chemotherapy resistance mechanisms of lipid metabolism reprogramming in leukemia cells, and summarizes the latest findings on targeted fatty acid metabolism pathways, aiming to provide a new perspective on the role of intracellular fatty acid metabolism in the occurrence and development of acute leukemia. It is expected to provide a theoretical basis for the elucidation of its resistance mechanism and the development of corresponding targeted therapies.
Coronary artery disease (CAD) is a cardiovascular disease mainly caused by atherosclerosis, which involves a variety of pathophysiological mechanisms such as lipid metabolism, inflammatory response, and endothelial dysfunction. Fetuin B is a glycoprotein secreted by the liver, which can participate in many processes such as cell inflammation, vascular calcification, and lipid metabolism, and is closely related to the pathogenesis of CAD. This article reviews the relationship between fetuin B and CAD and the mechanism of its occurrence and development, in order to provide new choices and methods for the prevention, diagnosis, and treatment of CAD.