scholarly journals Corrigendum to “Reduced Oxidative Stress Contributes to the Lipid Lowering Effects of Isoquercitrin in Free Fatty Acids Induced Hepatocytes”

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Waseem Hassan ◽  
Gao Rongyin ◽  
Abdelkader Daoud ◽  
Lin Ding ◽  
Lulu Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Lipid Lowering

scholarly journals Reduced Oxidative Stress Contributes to the Lipid Lowering Effects of Isoquercitrin in Free Fatty Acids Induced Hepatocytes

2014 ◽  
Vol 2014 ◽  
pp. 1-18 ◽  
Author(s):  
Waseem Hassan ◽  
Gao Rongyin ◽  
Abdelkader Daoud ◽  
Lin Ding ◽  
Lulu Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Lipid Metabolism ◽  
Free Fatty Acids ◽  
Molecular Level ◽  
Lipid Lowering ◽  
Hepatic Lipid Metabolism ◽  
Ampk Pathway ◽  
Coculture Model ◽  
And Oxidative Stress

Oxidative stress interferes with hepatic lipid metabolism at various levels ranging from benign lipid storage to so-called second hit of inflammation activation. Isoquercitrin (IQ) is widely present flavonoid but its effects on hepatic lipid metabolism remain unknown. We used free fatty acids (FFA) induced lipid overload and oxidative stress model in two types of liver cells and measured cell viability, intracellular lipids, and reactive oxygen species (ROS) within hepatocytes. In addition, Intracellular triglycerides (TG), superoxide dismutase (SOD), and malondialdehyde (MDA) were examined. A novelin vitromodel was used to evaluate correlation between lipid lowering and antioxidative activities. Furthermore, 34 major cytokines and corresponding ROS levels were analyzed in FFA/LPS induced coculture model between hepatocytes and Kupffer cells. At molecular level AMPK pathway was elucidated. We showed that IQ attenuated FFA induced lipid overload and ROS within hepatocytes. Further, IQ reversed FFA induced increase in intracellular TG SOD and MDA. It was shown that antioxidative activity of IQ correlates with its lipid lowering potentials. IQ reversed major proinflammatory cytokines and oxidative stress in FFA/LPS induced coculture model. Finally, AMPK pathway was found responsible for metabolic benefits at molecular level. IQ strikingly manifests antioxidative and related lipid lowering activities in hepatocytes.

scholarly journals Free Fatty Acids Impair FGF21 Action in HepG2 Cells

2015 ◽  
Vol 37 (5) ◽  
pp. 1767-1778 ◽  
Author(s):  
Mohamed Asrih ◽  
Christophe Montessuit ◽  
Jacques Philippe ◽  
François R. Jornayvaz
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Lipid Metabolism ◽  
Free Fatty Acids ◽  
Hepg2 Cells ◽  
Lipid Lowering ◽  
Fibroblast Growth Factor 21 ◽  
Beneficial Effects ◽  
Positive Effects

Background/Aims: Fibroblast growth factor 21 (FGF21) is a key mediator of glucose and lipid metabolism. However, the beneficial effects of exogenous FGF21 administration are attenuated in obese animals and humans with elevated levels of circulating free fatty acids (FFA). Methods: We investigated in vitro how FFA impact FGF21 effects on hepatic lipid metabolism. Results: In the absence of FFA, FGF21 reduced lipogenesis and increased lipid oxidation in HepG2 cells. Inhibition of lipogenesis was associated with a down regulation of SREBP-1c, FAS and SCD1. The lipid-lowering effect was associated with AMPK and ACC phosphorylation, and up regulation of CPT-1α expression. Further, FGF21 treatment reduced TNFα gene expression, suggesting a beneficial action of FGF21 on inflammation. In contrast, the addition of FFA abolished the positive effects of FGF21 on lipid metabolism. Conclusion: In the absence of FFA, FGF21 improves lipid metabolism in HepG2 cells and reduces the inflammatory cytokine TNFα. However, under high levels of FFA, FGF21 action on lipid metabolism and TNFα gene expression is impaired. Therefore, FFA impair FGF21 action in HepG2 cells potentially through TNFα.

Oxidative Stress Is Activated by Free Fatty Acids in Cultured Human Hepatocytes

2011 ◽  
Vol 9 (5) ◽  
pp. 397-401 ◽  
Author(s):  
Giorgio Soardo ◽  
Debora Donnini ◽  
Liana Domenis ◽  
Cristiana Catena ◽  
Daniele De Silvestri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Human Hepatocytes

scholarly journals Effect of High-Fat Diets on Oxidative Stress, Cellular Inflammatory Response and Cognitive Function

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2579 ◽  
Author(s):  
Bee Ling Tan ◽  
Mohd Esa Norhaizan
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Cognitive Dysfunction ◽  
Molecular Mechanisms ◽  
Cell Mediated Immunity ◽  
Low Grade ◽  
High Fat ◽  
Cellular Inflammatory Response

Cognitive dysfunction is linked to chronic low-grade inflammatory stress that contributes to cell-mediated immunity in creating an oxidative environment. Food is a vitally important energy source; it affects brain function and provides direct energy. Several studies have indicated that high-fat consumption causes overproduction of circulating free fatty acids and systemic inflammation. Immune cells, free fatty acids, and circulating cytokines reach the hypothalamus and initiate local inflammation through processes such as microglial proliferation. Therefore, the role of high-fat diet (HFD) in promoting oxidative stress and neurodegeneration is worthy of further discussion. Of particular interest in this article, we highlight the associations and molecular mechanisms of HFD in the modulation of inflammation and cognitive deficits. Taken together, a better understanding of the role of oxidative stress in cognitive impairment following HFD consumption would provide a useful approach for the prevention of cognitive dysfunction.

scholarly journals Ginsenoside Rb1 inhibits free fatty acids-induced oxidative stress and inflammation in 3T3-L1 adipocytes

2017 ◽  
Vol 16 (6) ◽  
pp. 9165-9172 ◽  
Author(s):  
Min Wang ◽  
Yanming Chen ◽  
Zhaojun Xiong ◽  
Shujie Yu ◽  
Bin Zhou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Ginsenoside Rb1

scholarly journals GENDER-RELATED ALTERATIONS IN FREE FATTY ACIDS AND OXIDATIVE STRESS IN HYPERTENSION CO-MORBIDLY OCCURRING WITH TYPE 2 DIABETES MELLITUS

2019 ◽  
Vol 16 (2) ◽  
pp. 26-38
Author(s):  
A. J. AKAMO ◽  
R. N. UGBAJA ◽  
O. ADEMUYIWA ◽  
D. I. AKINLOYE ◽  
O. T. SOMADE ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Type 2 Diabetes Mellitus ◽  
Free Fatty Acids ◽  
Female Patients ◽  
And Oxidative Stress ◽  
Plasma Ffas

Increase in plasma free fatty acids (FFAs) concentrations may cause cellular damage via the induction of oxidative stress. The aim of this present study was to investigate FFAs and oxidative stress in hypertension co-morbidly occurring with Type 2 Diabetes Mellitus (T2DM). Age and sex matched control subjects (n=150) and patients (n=470) [hypertensive nondiabetics (HND, n=179), normotensive diabetics (ND, n=132), hypertensive diabetics (HD, n=159)] presenting at the Medical Out-Patient Clinic of the State Hospital, Abeokuta, Nigeria were recruited. Fasting plasma glucose, creatinine, urea, FFAs, thiobarbituric acid reactive substances (TBARS) were determined spectrophotometrically. The presence of either or both diseases resulted in significant increase (p<0.05) in the plasma FFAs and oxidative stress marker-TBARS in different compartments (plasma, erythrocytes andlipoproteins) for both male and female patients when compared with their control counterparts. The increase in FFAs was more marked in comorbidity female when compared with other female patients. There was significant (p<0.05) difference in gender FFAs concentrations. In both controls and patients, FFAs in plasma are significantly (p<0.05) higher in male when compared with their female counterparts. This research revealed biochemical variations in hypertension co-morbidly occurring with T2DMcharacterised by gender-related elevation in FFAs and enhanced oxidative stress. Plasma FFAs might be a good biomarker predicting the occurrence and development of hypertension and/or T2DM.  

scholarly journals Regular Dark Chocolate Consumption’s Reduction of Oxidative Stress and Increase of Free-Fatty-Acid Mobilization in Response to Prolonged Cycling

2011 ◽  
Vol 21 (2) ◽  
pp. 113-123 ◽  
Author(s):  
Judith Allgrove ◽  
Emily Farrell ◽  
Michael Gleeson ◽  
Gary Williamson ◽  
Karen Cooper
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Treatment Time ◽  
Venous Blood ◽  
Dark Chocolate ◽  
Plasma Metabolites ◽  
Time To Exhaustion ◽  
Before And After ◽  
Markers Of Oxidative Stress

This study investigated the effects of regular consumption of dark chocolate (DC), rich in cocoa polyphenols, on plasma metabolites, hormones, and markers of oxidative stress after prolonged exhaustive exercise. Twenty active men cycled at 60% maximal oxygen uptake (VO2max) for 1.5 hr, with the intensity increased to 90% VO2max for a 30-s period every 10 min, followed by a ride to exhaustion at 90% VO2max. In the 2 wk before exercise participants consumed 40 g of DC or an isocarbohydrate-fat control cocoa liquor–free chocolate (CON) twice daily and once 2 hr before exercise in a randomized, counterbalanced, crossover design. Venous blood samples were taken immediately before exercise, postexercise (fixed duration), postexhaustion, and after 1 hr of recovery. F2-isoprostanes were significantly lower (post hoc tests: p < .001) at exhaustion and after 1 hr of recovery with DC. Oxidized low-density lipoproteins were significantly lower with DC (p < .001) both before and after exercise and at exhaustion. DC was also associated with ~21% greater rises in free fatty acids during exercise (main effect: p < .05). Changes in circulating glucose, insulin, glucagon, cortisol, and interleukin (IL)-6, IL-10, and IL-1ra were unaffected by treatment. Time to exhaustion at 90% VO2max was not significantly different between trials (398 ± 204 and 374 ± 194 s for DC and CON, respectively). These results suggest that regular DC intake is associated with reduced oxidative-stress markers and increased mobilization of free fatty acids after exercise but has no observed effect on exercise performance.

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