scholarly journals Transcriptional Control by HNF-1: Emerging Evidence Showing Its Role in Lipid Metabolism and Lipid Metabolism Disorders

2021 ◽  
Author(s):  
Fang Liu ◽  
Xiao Zhu ◽  
Xiaping Jiang ◽  
Shan Li ◽  
Yuncheng Lv
Keyword(s):  
Lipid Metabolism ◽  
Transcriptional Control ◽  
Lipid Metabolism Disorders

The correlation between lipid metabolism disorders and the prostate cancer

2020 ◽  
Vol 27 ◽  
Author(s):  
Justyna Dłubek ◽  
Jacek Rysz ◽  
Zbigniew Jabłonowski ◽  
Anna Gluba-Brzózka ◽  
Beata Franczyk
Keyword(s):  
Prostate Cancer ◽  
Fatty Acids ◽  
Lipid Metabolism ◽  
Cancer Progression ◽  
De Novo ◽  
Prostate Gland ◽  
Hdl Cholesterol ◽  
Atp Citrate Lyase ◽  
Male Population ◽  
Lipid Metabolism Disorders

: Prostate cancer is second most common cancer affecting male population all over the world. The existence of a correlation between lipid metabolism disorders and cancer of the prostate gland has been widely known for a long time. According to hypotheses, cholesterol may contribute to prostate cancer progression as a result of its participation as a signalling molecule in prostate growth and differentiation via numerous biologic mechanisms including Akt signalling and de novo steroidogenesis. The results of some studies suggest that increased cholesterol levels may be associated with higher risk of more aggressive course of disease. The aforementioned alterations in the synthesis of fatty acids are a unique feature of cancer and, therefore, it constitutes an attractive target for therapeutic intervention in the treatment of prostate cancer. Pharmacological or gene therapy aimed to reduce the activity of enzymes involved in de novo synthesis of fatty acids, FASN, ACLY (ATP citrate lyase) or SCD-1 (stearoyl-CoA desaturase) in particular, may result in cells growth arrest. Nevertheless, not all cancers are unequivocally associated with hypocholesterolaemia. It cannot be ruled out that the relationship between prostate cancer and lipid disorders is not a direct quantitative correlation between carcinogenesis and the amount of the circulating cholesterol. Perhaps the correspondence is more sophisticated and connected to the distribution of cholesterol fractions, or even sub-fractions of e.g. HDL cholesterol.

scholarly journals AB0875-HPR NON-PHARMACOLOGICAL AND PHARMACOLOGICAL APPROACHES TO THE MANAGEMENT OF PATIENTS WITH OSTEOARTHRITIS AND LIPID METABOLISM DISORDERS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1461.1-1461
Author(s):  
T. Rogatkina ◽  
O. Korolik ◽  
V. Polyakov ◽  
G. Kravtsov ◽  
Y. Polyakova
Keyword(s):  
Physical Activity ◽  
Cardiovascular Disease ◽  
Lipid Metabolism ◽  
Lipid Profile ◽  
Fat Mass ◽  
Prognostic Significance ◽  
Lipid Lowering ◽  
Lipid Lowering Therapy ◽  
Lipid Metabolism Disorders ◽  
Group I

Background:Attention is drawn to the frequent combination of osteoarthritis (OA) with cardiovascular disease. Non-specific inflammation plays a significant role in the pathogenesis of OA and atherosclerosis. Limiting the physical activity of patients with OA is an additional important factor aggravating the course of cardiovascular disease (CVD). Chronic pain syndrome, causing a neuroendocrine response, is often the cause of the development of complications of atherosclerotic disease. Dyslipidemia is the main cause of atherosclerosis and vascular thrombosis.Objectives:To study variants of lipid metabolism disorders in female and male patients of different age groups with osteoarthritis.Methods:Case histories of 90 patients with OA were analyzed. The average age of patients was 63.27 ± 11.31 years. The average body mass index (BMI) is 39.8 ± 3.2. All patients underwent questionnaires, general clinical and biochemical blood tests with lipid profile determination, anthropometry, bioimpedansometry, and the main metabolic rate assessment using indirect calorimetry in dynamics (at the beginning of the study and after 3 months).Results:Burdened heredity for obesity, arterial hypertension (AH), diabetes mellitus (DM) was revealed. AH was diagnosed in 76 patients (84.4%), type II diabetes in 17 (18.9%), dyslipidemia and hypercholesterolemia in 56 (62.2%). Statins were taken by 43 patients (47.8%) - group I patients, which is associated with low adherence to therapy, group II included patients who did not initially take statins or stopped taking them at least 6 months before inclusion in the study.Against the background of diet therapy and physiotherapy exercises, BMI (R0.99; p <0.05), fat mass (R0.95; p <0.05) significantly decreased, lipid profile normalization was noted: total cholesterol (R0.66; p <0 .05), LDL (R0.69; p <0.05), HDL (R0.95; p <0.05), TG (R0.57; p <0.05), AST decreased (R0.64; p <0.05) and ALT (R0.76; p <0.05) in both groups of patients, regardless of lipid-lowering therapy. A decrease in fat mass correlated with TG levels (R0.51; p <0.05), an increase in skeletal muscle mass (R0.60; p <0.05), lean mass (R0.72; p <0.05), and active cell mass (R0.59; p <0.05). The lipid profile in the I group of patients was significantly better before and at the end of the study. Long-term effects have not been investigated due to the short duration of the study.Conclusion:In patients with OA, a high frequency of concomitant diseases of the cardiovascular system, lipid metabolism disorders was found. Non-drug therapy has a positive effect on the lipid profile and the level of transaminases. The decrease in body weight due to loss of fat mass reliably correlates with the level of TG. Timely use of statins contributes to the normalization of the lipid profile, reduces the risk of cardiovascular disease in patients with OA. It is necessary to study lipid profile disorders in patients with OA with recommendations for lifestyle modification (diet, physical activity), and if necessary, prescribe lipid-correcting therapy.References:[1]E. Simakova, B. Zavodovsky, L. Sivordova [et al]. Prognostic significance of lipid disorders markers determination in pathogenesis of osteoarthritis. Vestnik Rossijskoj voenno-medicinskoj akademii. 2013. No. 2 (42). P.29-32.[2]Zavodovsky B.V., Sivordova L.E. Prognostic significance value of definition of leptin level determination in osteoarthritis. Siberian Medical Journal (Irkutsk). 2012; 115(8):069-072.Disclosure of Interests:None declared

Effects of VO2 nanoparticles on human liver HepG2 cells: Cytotoxicity, genotoxicity, and glucose and lipid metabolism disorders

NanoImpact ◽  
2021 ◽  
Vol 24 ◽  
pp. 100351
Author(s):  
Jia-Bei Li ◽  
Wen-Song Xi ◽  
Shi-Ying Tan ◽  
Yuan-Yuan Liu ◽  
Hao Wu ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Glucose And Lipid Metabolism ◽  
Lipid Metabolism Disorders

scholarly journals MicroRNA-33-5p inhibits cholesterol efflux in vascular endothelial cells by regulating citrate synthase and ATP-binding cassette transporter A1

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Qiong Xie ◽  
Jianqiang Peng ◽  
Ying Guo ◽  
Feng Li
Keyword(s):  
Endothelial Cells ◽  
Lipid Metabolism ◽  
Cholesterol Efflux ◽  
Citrate Synthase ◽  
Vascular Endothelial Cells ◽  
Density Lipoprotein ◽  
Atp Binding ◽  
Vascular Endothelial ◽  
Lipid Metabolism Disorders ◽  
Atp Binding Cassette

Abstract Background A high level of total cholesterol is associated with several lipid metabolism disorders, including atherosclerosis and cardiovascular diseases. ATP-binding cassette (ABC) transporter A1 (ABCA1) and miR-33-5p play crucial roles in atherosclerosis by controlling cholesterol efflux. While citrate is a precursor metabolite for lipid and cholesterol synthesis, little is known about the association between citrate synthase (CS) and cholesterol efflux. This study investigated the role of the miR-33-5p/ABCA1/CS axis in regulating cholesterol efflux in vascular endothelial cells (VECs). Materials and methods VECs were treated with oxidized low-density lipoprotein cholesterol (ox-LDL), or pretreated with plasmids overexpressing CS, ABCA1, siRNAs against CS and ABCA1, and an miR-33-5p inhibitor. Cell apoptosis, cellular senescence-associated β-galactosidase activity, inflammation, and cholesterol efflux were detected. Results Treatment with ox-LDL decreased ABCA1 and CS levels and increased miR-33-5p expression and apoptosis in dose-dependent manners. In contrast, treatment with the miR-33-5p inhibitor and ABCA1 and CS overexpression plasmids inhibited the above-mentioned ox-LDL-induced changes. In addition, treatment with ox-LDL decreased cholesterol efflux, induced aging, and promoted the production of inflammatory cytokines (i.e., IL-6 and tumor necrosis factor TNF-α), as well as the expression of Bax and Caspase 3 proteins in VECs. All these changes were rescued by miR-33-5p inhibition and ABCA1 and CS overexpression. The inhibition of ABCA1 and CS by siRNAs eliminated the effects mediated by the miR-33-5p inhibitor, and knockdown of CS eliminated the effects of ABCA1 on VECs. Conclusions This study demonstrated the crucial roles played by the miR-33-5p/ABCA1/CS axis in regulating cholesterol efflux, inflammation, apoptosis, and aging in VECs, and also suggested the axis as a target for managing lipid metabolism disorders.

SEX DIFFERENCES OF CARBOHYDRATE AND LIPID METABOLISM IMPAIRMENT IN RATS WITH TYPE 2 DIABETES MELLITUS

2018 ◽  
Vol 64 (2) ◽  
pp. 39-45 ◽  
Author(s):  
Nataliia Gorbenko ◽  
Oleksii Borikov ◽  
Olha Ivanova ◽  
K. V. Taran ◽  
T. S. Litvinova ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Body Weight ◽  
Lipid Metabolism ◽  
Female Rats ◽  
Glucose And Lipid Metabolism ◽  
Carbohydrate And Lipid Metabolism ◽  
Lipid Metabolism Disorders

A sex difference of carbohydrate and lipid metabolism disorders in rats with type 2 diabetes has been studied. It was established that type 2 diabetes leads to a more pronounced deterioration in carbohydrate toleranceand insulin sensitivity in males compared to female rats, but the sex doesn’t affect basal glycemia and fructosamine levels. It was found that the increase of body weight and visceral fat in rats with type 2 diabetes is moremanifested in females than in males. It has been determined that hypertriglyceridemia is higher in diabeticmales compared to diabetic females, and the level of common lipids in the liver, both intact females and femaleswith type 2 diabetes, is lower than that of the males. The obtained results indicate a more expressive impairment of glucose and lipid metabolism in males compared to females with type 2 diabetes

Abstract 5276: Sumoylation Of Klf5 Is A Molecular Switch Regulating Ppar-δ-containing Transcriptional Programs Of Lipid Metabolism

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Yumiko Oishi ◽  
Ichiro Manabe ◽  
Kazuyuki Tobe ◽  
Takashi Kadowaki ◽  
Ryozo Nagai
Keyword(s):  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Lipid Metabolism ◽  
Cardiovascular Diseases ◽  
Transcriptional Control ◽  
Uncoupling Protein ◽  
Molecular Switch ◽  
Atherosclerotic Cardiovascular Disease ◽  
Transcriptional Regulatory ◽  
Reporter Assays

Metabolic syndrome is increasingly recognized as a major risk factor for cardiovascular disease. We have previously shown that a zinc finger transcription factor, Krüppel-like factor 5 (KLF5), plays an important role in cardiovascular diseases, such as atherosclerosis and cardiac hypertrophy. Interestingly, KLF5 is also expressed in metabolic tissues, such as adipose tissue, skeletal muscle and pancreatic β-cells. Moreover, we found that KLF5 is crucial for adipocyte differentiation. Therefore, it is very likely that KLF5 plays multiple roles in development and progression of metabolic syndrome and its cardiovascular and metabolic consequences including atherosclerotic cardiovascular disease. Indeed, KLF5 heterozygous knockout ( KLF5 +/− ) mice were resistant to high-fat-induced obesity and metabolic syndrome, despite consuming more food than wild-type mice. This appears to in part reflect their enhanced energy expenditure. Expression of the genes involved in lipid oxidation and energy uncoupling, including uncoupling protein (UCP) and carnitine-palmitoyl transferase 1b (CPT1b) was upregulated in the soleus muscles of KLF5 +/− mice. KLF5 could be reversibly modified by small ubiquitin-like modifier 1 (SUMO1), after which SUMOylated KLF5 strongly inhibited CPT1b , UCP3 and UCP2 promoter activity. Results of chromatin immunoprecipitation, two-hybrid, and reporter assays showed that under basal conditions SUMOylated KLF5 associated with transcriptionally repressive regulatory complexes containing unliganded PPARδ and corepressors. However, upon agonist stimulation of PPARδ, the deSUMOylating enzyme was recruited and KLF5 was deSUMOylated. The unSUMOylated KLF5 now formed transactivating complexes with liganded PPARδ and CBP. Thus, SUMOylation appears to be a molecular switch affecting function of KLF5 and the transcriptional regulatory programs governing lipid metabolism. Moreover, KLF5 is essential for the PPARδ agonist-dependent transcriptional control. Results of the present study have established KLF5 as a novel key molecule in lipid metabolism and suggest that the posttranscriptional modification of KLF5 is an attractive novel therapeutic target for both metabolic and cardiovascular diseases.

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