scholarly journals Impact of broiler egg storage on the relative expression of selected blastoderm genes associated with apoptosis, oxidative stress, and fatty acid metabolism

2016 ◽  
Vol 95 (6) ◽  
pp. 1411-1417 ◽  
Author(s):  
M.R. Bakst ◽  
G.R. Welch ◽  
R. Fetterer ◽  
K. Miska
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Relative Expression ◽  
Egg Storage

scholarly journals Phenolic Compounds Reduce the Fat Content in Caenorhabditis elegans by Affecting Lipogenesis, Lipolysis, and Different Stress Responses

2020 ◽  
Vol 13 (11) ◽  
pp. 355
Author(s):  
Paula Aranaz ◽  
David Navarro-Herrera ◽  
María Zabala ◽  
Ana Romo-Hualde ◽  
Miguel López-Yoldi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Phenolic Compounds ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Lipid Mobilization ◽  
C Elegans ◽  
Unfolded Protein ◽  
Reducing Activity ◽  
Protein Response

Supplementation with bioactive compounds capable of regulating energy homeostasis is a promising strategy to manage obesity. Here, we have screened the ability of different phenolic compounds (myricetin, kaempferol, naringin, hesperidin, apigenin, luteolin, resveratrol, curcumin, and epicatechin) and phenolic acids (p-coumaric, ellagic, ferulic, gallic, and vanillic acids) regulating C. elegans fat accumulation. Resveratrol exhibited the strongest lipid-reducing activity, which was accompanied by the improvement of lifespan, oxidative stress, and aging, without affecting worm development. Whole-genome expression microarrays demonstrated that resveratrol affected fat mobilization, fatty acid metabolism, and unfolded protein response of the endoplasmic reticulum (UPRER), mimicking the response to calorie restriction. Apigenin induced the oxidative stress response and lipid mobilization, while vanillic acid affected the unfolded-protein response in ER. In summary, our data demonstrates that phenolic compounds exert a lipid-reducing activity in C. elegans through different biological processes and signaling pathways, including those related with lipid mobilization and fatty acid metabolism, oxidative stress, aging, and UPR-ER response. These findings open the door to the possibility of combining them in order to achieve complementary activity against obesity-related disorders.

Tibolone impairs glucose and fatty acid metabolism and induces oxidative stress in livers from female rats

2011 ◽  
Vol 668 (1-2) ◽  
pp. 248-256 ◽  
Author(s):  
Monique C. de Oliveira ◽  
Elismari R. Martins-Maciel ◽  
Jurandir F. Comar ◽  
Nair S. Yamamoto ◽  
Adelar Bracht ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Female Rats

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

scholarly journals RiboTag translatomic profiling of Drosophila oenocytes under aging and oxidative stress

2018 ◽  
Author(s):  
Kerui Huang ◽  
Wenhao Chen ◽  
Fang Zhu ◽  
Hua Bai
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Stress Response ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Fat Body ◽  
Mapk Signaling ◽  
Age Related ◽  
And Oxidative Stress

AbstractBackgroundAging is accompanied with loss of tissue homeostasis and accumulation of cellular damages. As one of the important metabolic centers, aged liver shows altered lipid metabolism, impaired detoxification pathway, increased inflammation and oxidative stress response. However, the mechanisms for these age-related changes still remain unclear. In fruit flies, Drosophila melanogaster, liver-like functions are controlled by two distinct tissues, fat body and oenocytes. Although the role of fat body in aging regulation has been well studied, little is known about how oenocytes age and what are their roles in aging regulation. To address these questions, we used cell-type-specific ribosome profiling (RiboTag) to study the impacts of aging and oxidative stress on oenocyte translatome in Drosophila.ResultsWe show that aging and oxidant paraquat significantly increased the levels of reactive oxygen species (ROS) in adult oenocytes of Drosophila, and aged oenocytes exhibited reduced sensitivity to paraquat treatment. Through RiboTag sequencing, we identified 3324 and 949 differentially expressed genes in oenocytes under aging and paraquat treatment, respectively. Aging and paraquat exhibit both shared and distinct regulations on oenocyte translatome. Among all age-regulated genes, mitochondrial, proteasome, peroxisome, fatty acid metabolism, and cytochrome P450 pathways were down-regulated, whereas DNA replication and glutathione metabolic pathways were up-regulated. Interestingly, most of the peroxisomal genes were down-regulated in aged oenocytes, including peroxisomal biogenesis factors and beta-oxidation genes. Further analysis of the oenocyte translatome showed that oenocytes highly expressed genes involving in liver-like processes (e.g., ketogenesis). Many age-related transcriptional changes in oenocytes are similar to aging liver, including up-regulation of Ras/MAPK signaling pathway and down-regulation of peroxisome and fatty acid metabolism.ConclusionsOur oenocyte-specific translatome analysis identified many genes and pathways that are shared between Drosophila oenocytes and mammalian liver, highlighting the molecular and functional similarities between the two tissues. Many of these genes are altered in both aged oenocytes and aged liver, suggesting a conserved molecular mechanism underlying oenocyte and liver aging. Thus, our translatome analysis will contribute significantly to the understanding of oenocyte biology, and its role in lipid metabolism, stress response and aging regulation.

scholarly journals HSP60 Regulates Lipid Metabolism in Human Ovarian Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-21
Author(s):  
Na Li ◽  
Nannan Li ◽  
Siqi Wen ◽  
Biao Li ◽  
Yaying Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ovarian Cancer ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Pathway Network

Accumulating evidence demonstrates that cancer is an oxidative stress-related disease, and oxidative stress is closely linked with heat shock proteins (HSPs). Lipid oxidative stress is derived from lipid metabolism dysregulation that is closely associated with the development and progression of malignancies. This study sought to investigate regulatory roles of HSPs in fatty acid metabolism abnormality in ovarian cancer. Pathway network analysis of 5115 mitochondrial expressed proteins in ovarian cancer revealed various lipid metabolism pathway alterations, including fatty acid degradation, fatty acid metabolism, butanoate metabolism, and propanoate metabolism. HSP60 regulated the expressions of lipid metabolism proteins in these lipid metabolism pathways, including ADH5, ECHS1, EHHADH, HIBCH, SREBP1, ACC1, and ALDH2. Further, interfering HSP60 expression inhibited migration, proliferation, and cell cycle and induced apoptosis of ovarian cancer cells in vitro. In addition, mitochondrial phosphoproteomics and immunoprecipitation-western blot experiments identified and confirmed that phosphorylation occurred at residue Ser70 in protein HSP60, which might regulate protein folding of ALDH2 and ACADS in ovarian cancers. These findings clearly demonstrated that lipid metabolism abnormality occurred in oxidative stress-related ovarian cancer and that HSP60 and its phosphorylation might regulate this lipid metabolism abnormality in ovarian cancer. It opens a novel vision in the lipid metabolism reprogramming in human ovarian cancer.

scholarly journals Effects of Di-(2-Ethylhexyl) Phthalate At Environmentally Relevant Concentrations On Oxidative Stress and Lipid Metabolism in Livers of Male Xenopus Tropicalis

2021 ◽  
Author(s):  
Xinying Pan ◽  
Li Zheng ◽  
Yong Ding ◽  
Zhuo Dai ◽  
Xufeng Qi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Aquatic Organisms ◽  
Mitochondrial Morphology ◽  
Histopathological Analysis ◽  
Expression Of Genes ◽  
Ethylhexyl Phthalate ◽  
Dehp Exposure

Abstract Di-(2-ethylhexyl) phthalate (DEHP), used as a popular plasticizer to enhance the flexibility of plastics, is a major pollutant in aquatic environments. DEHP poses severe risks to aquatic organisms since it is an endocrine-disrupting compound. To comprehensively evaluate the toxicity of DEHP on the growth and livers of male X. tropicalis, sexually mature male X. tropicalis were exposed to environmentally relevant concentrations of DEHP, 0.2, 0.6, 1.8, 5.4 mg/L, for 49 days. The results showed that DEHP had a severe toxic effect on the livers of male X. tropicalis. Histopathological analysis of livers in all the DEHP-exposed groups showed changes in terms of vacuolization, loose cell cords, and an increasing amount of melanin. Large lipid droplets were markedly formed, and there were changes in the mitochondrial morphology upon DEHP exposure. In addition, oxidative stress was induced through the suppression of biochemical indicators and the downregulation in the mRNA expression of genes (nrf2, cat, sod, gst, and gpx) related to oxidative stress. A reduction in expression of fatty acid metabolism-related genes (pparα) was seen post-DEHP exposure. Thus, our study suggests that the hepatotoxicity induced by DEHP could be attributed to oxidative stress and disordered fatty acid metabolism. In conclusion, long-term exposure to DEHP at environmentally relevant concentrations poses ecological risks to aquatic organisms, which serves as a reminder that the application of DEHP and other plasticizers should be limited.

scholarly journals Efficacy of Novavit in ameliorating the neurotoxicity of propionic acid

2020 ◽  
Vol 11 (1) ◽  
pp. 134-146
Author(s):  
Sarah I. Bukhari ◽  
Hanan Alfawaz ◽  
Abeer Al-Dbass ◽  
Ramesa Shafi Bhat ◽  
Nadine MS Moubayed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Fatty Acid ◽  
Gut Microbiota ◽  
Propionic Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Albino Rats ◽  
Oral Supplementation ◽  
Impaired Fatty Acid

AbstractOxidative stress, abnormal fatty acid metabolism, and impaired gut microbiota play a serious role in the pathology of autism. The use of dietary supplements to improve the core symptoms of autism is a common therapeutic strategy. The present study analyzed the effects of oral supplementation with Novavit, a multi-ingredient supplement, on ameliorating oxidative stress and impaired lipid metabolism in a propionic acid (PPA)-induced rodent model of autism. Male western albino rats were divided into three groups. The first group is the control, the second group was given an oral neurotoxic dose of PPA (250 mg/kg body weight/day) for 3 days and then received buffered saline until the end of the experiment. The third group received Novavit (70 mg/kg body weight/day for 30 days after the 3-day PPA treatment). Markers of oxidative stress and impaired fatty acid metabolism were measured in brain homogenates obtained from each group. Novavit modulation of the gut microbiota was also evaluated. While PPA induced significant increases in lipid peroxides and 5-lipoxygenase, together with significantly decreased glutathione, and cyclooxygenase 2, oral supplementation with Novavit ameliorated PPA-induced oxidative stress and impaired fatty acid metabolism. Our results showed that the presence of multivitamins, coenzyme Q10, minerals, and colostrum, the major components of Novavit, protects against PPA-induced neurotoxicity.

Abstract 271: Reduced Expression of the Cardiac Sodium Channel Nav1.5 Triggers Enhanced Fatty Acid Metabolism and Oxidative Stress

2019 ◽  
Vol 125 (Suppl_1) ◽  
Author(s):  
Ryan L Boudreau ◽  
Xiaoming Zhang ◽  
Jared M McLendon ◽  
William Kutschke ◽  
Ethan J Anderson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Sodium Channel ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Cardiac Sodium Channel ◽  
And Oxidative Stress
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