scholarly journals Pathway Preferential Estrogens Prevent Hepatosteatosis Due to Ovariectomy and High−Fat Diets

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3334
Author(s):  
Qianying Zuo ◽  
Karen L. Chen ◽  
Alicia Arredondo Arredondo Eve ◽  
Yu-Jeh Liu ◽  
Sung Hoon Kim ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Postmenopausal Women ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Metabolic Health ◽  
Plasma Metabolites ◽  
Collagen Deposition ◽  
Metabolomics Data ◽  
Increased Risk

About 20–30% of premenopausal women have metabolic syndrome, and the number is almost double in postmenopausal women, and these women have an increased risk of hepatosteatosis. Postmenopausal women with metabolic syndrome are often treated with hormone replacement therapy (HRT), but estrogens in currently available HRTs increase the risk of breast and endometrial cancers and Cardiovascular Disease. Therefore, there is a critical need to find safer alternatives to HRT to improve postmenopausal metabolic health. Pathway preferential estrogen 1 (PaPE−1) is a novel estrogen receptor ligand that has been shown to favorably affect metabolic tissues without adverse effects on reproductive tissues. In this study, we have examined the effects of PaPE−1 on metabolic health, in particular, examining its effects on the liver transcriptome and on plasma metabolites in two different mouse models: diet−induced obesity (DIO) and leptin−deficient (ob/ob) mice. PaPE−1 significantly decreased liver weight and lipid accumulation in both DIO and ob/ob models and lowered the expression of genes associated with fatty acid metabolism and collagen deposition. In addition, PaPE−1 significantly increased the expression of mitochondrial genes, particularly ones associated with the electron transport chain, suggesting an increase in energy expenditure. Integrated pathway analysis using transcriptomics and metabolomics data showed that PaPE−1 treatment lowered inflammation, collagen deposition, and pathways regulating fatty acid metabolism and increased metabolites associated with glutathione metabolism. Overall, our findings support a beneficial metabolic role for PaPE−1 and suggest that PaPE−1 may protect postmenopausal women from fatty liver disease without increasing reproductive cancer risk.

scholarly journals Severity of Metabolic Syndrome Unfavorably Influences Oxidative Stress and Fatty Acid Metabolism in Men

2007 ◽  
Vol 212 (4) ◽  
pp. 359-371 ◽  
Author(s):  
Aleš Zák ◽  
Eva Tvrzická ◽  
Marek Vecka ◽  
Marie Jáchymová ◽  
Ladislava Duffková ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism

Inflammation, obesity, and fatty acid metabolism: influence ofn-3 polyunsaturated fatty acids on factors contributing to metabolic syndrome

2007 ◽  
Vol 32 (6) ◽  
pp. 1008-1024 ◽  
Author(s):  
Lindsay E. Robinson ◽  
Andrea C. Buchholz ◽  
Vera C. Mazurak
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acids ◽  
Abdominal Obesity ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Preliminary Evidence ◽  
Postprandial Period

Metabolic syndrome (MetS) comprises an array of metabolic risk factors including abdominal obesity, dyslipidemia, hypertension, and glucose intolerance. Individuals with MetS are at elevated risk for diabetes and cardiovascular disease. Central to the etiology of MetS is an interrelated triad comprising inflammation, abdominal obesity, and aberrations in fatty acid metabolism, coupled with the more recently recognized changes in metabolism during the postprandial period. We review herein preliminary evidence regarding the role of dietary n-3 polyunsaturated fatty acids in modulating each of the components of the triad of adiposity, inflammation, and fatty acid metabolism, with particular attention to the role of the postprandial period as a contributor to the pathophysiology of MetS.

scholarly journals Fatty acid metabolism and colon cancer protection by dietary methyl donor restriction

Metabolomics ◽  
2021 ◽  
Vol 17 (9) ◽  
Author(s):  
Oladimeji Aladelokun ◽  
Matthew Hanley ◽  
Jinjian Mu ◽  
John C. Giardina ◽  
Daniel W. Rosenberg ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Caloric Intake ◽  
Tumor Development ◽  
Positive Association ◽  
Plasma Metabolites ◽  
Methyl Donor ◽  
Cancer Suppression ◽  
Cancer Risk Reduction

Abstract Introduction A methyl donor depleted (MDD) diet dramatically suppresses intestinal tumor development in Apc-mutant mice, but the mechanism of this prevention is not entirely clear. Objectives We sought to gain insight into the mechanisms of cancer suppression by the MDD diet and to identify biomarkers of cancer risk reduction. Methods A plasma metabolomic analysis was performed on ApcΔ14/+ mice maintained on either a methyl donor sufficient (MDS) diet or the protective MDD diet. A group of MDS animals was also pair-fed with the MDD mice to normalize caloric intake, and another group was shifted from an MDD to MDS diet to determine the durability of the metabolic changes. Results In addition to the anticipated changes in folate one-carbon metabolites, plasma metabolites related to fatty acid metabolism were generally decreased by the MDD diet, including carnitine, acylcarnitines, and fatty acids. Some fatty acid selectivity was observed; the levels of cancer-promoting arachidonic acid and 2-hydroxyglutarate were decreased by the MDD diet, whereas eicosapentaenoic acid (EPA) levels were increased. Machine-learning elastic net analysis revealed a positive association between the fatty acid-related compounds azelate and 7-hydroxycholesterol and tumor development, and a negative correlation with succinate and β-sitosterol. Conclusion Methyl donor restriction causes dramatic changes in systemic fatty acid metabolism. Regulating fatty acid metabolism through methyl donor restriction favorably effects fatty acid profiles to achieve cancer protection.

scholarly journals Exploration the mechanism of doxorubicin-induced Heart failure in Rats by integration of proteomics and metabolomics data

2020 ◽  
Author(s):  
Yu Yuan ◽  
Simiao Fan ◽  
Lexin Shu ◽  
Wei Huang ◽  
Lijuan Xie ◽  
...  
Keyword(s):  
Heart Failure ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Molecular Mechanisms ◽  
Acid Metabolism ◽  
Systemic Disease ◽  
Cardiac Metabolism ◽  
Glutathione Metabolism ◽  
High Morbidity ◽  
Metabolomics Data

Abstract Background Heart failure is currently a worldwide systemic disease with high morbidity and mortality and is very common. At present, many studies have shown that heart failure is associated with obesity, hypertension and diabetes, but it is still unable to prevent the disease from progressing. Here, we elucidate the molecular mechanisms of doxorubicin–induced harmful effects on rat cardiac metabolism and function from a new perspective, using metabonomics and Proteomics analysis data. Methods The aim of this study was to use metabonomic and proteomic techniques to systematically elucidate the molecular mechanisms of doxorubicin (DOX)–induced heart failure (HF) in rat. In this study, we aimed to systematically elucidate the molecular action of Dox on rats heart and the reasons for DOX–induced the HF mechanism through the metabonomics tandem mass tag (TMT)–based quantitative proteomics approach. Rats were gavaged with DOX (3 mg/kg) for 6 weeks and the plasma metabonomics, cardiac tissue proteomics, histopathology and related proteins expression levels. Results A total of 278 proteins and 21 metabolites were significantly altered in rats following DOX treatments. The responsive proteins and metabolites were predominantly involved in Fatty acid metabolism, Glycolysis, glycerophospholipid metabolism, TCA cycle, Glutathione metabolism, Myocardial contraction. Conclusions The present study indicates the PTP1B inhibits the expression of HIF-1α by inhibiting the phosphorylation of IRS, leading to disorders of fatty acid metabolism and glycolysis, which together with the decrease of Nrf2, SOD, Cytc and AK4 proteins lead to oxidative stress, suggesting the PTP1B may serve as a potential target in the treatment of heart failure.

scholarly journals Fatty Acid CoA Ligase-4 Gene Polymorphism Influences Fatty Acid Metabolism in Metabolic Syndrome, but not in Depression

2009 ◽  
Vol 217 (4) ◽  
pp. 287-293 ◽  
Author(s):  
Miroslav Zeman ◽  
Marek Vecka ◽  
Marie Jáchymová ◽  
Roman Jirák ◽  
Eva Tvrzická ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Gene Polymorphism ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Coa Ligase

scholarly journals Deletion of NLRX1 increases fatty acid metabolism and prevents diet-induced hepatic steatosis and metabolic syndrome

2018 ◽  
Vol 1864 (5) ◽  
pp. 1883-1895 ◽  
Author(s):  
Lotte Kors ◽  
Elena Rampanelli ◽  
Geurt Stokman ◽  
Loes M. Butter ◽  
Ntsiki M. Held ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Hepatic Steatosis ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism
Sign in / Sign up

Export Citation Format

Share Document