scholarly journals Estrogen-Related Receptor α Inverse Agonist Enhances Basal Glucose Uptake in Myotubes through Reactive Oxygen Species

2009 ◽  
Vol 32 (7) ◽  
pp. 1199-1203 ◽  
Author(s):  
Lihua Chen ◽  
Chiwai Wong
Keyword(s):  
Reactive Oxygen Species ◽  
Glucose Uptake ◽  
Reactive Oxygen ◽  
Inverse Agonist ◽  
Oxygen Species ◽  
Estrogen Related Receptor ◽  
Basal Glucose Uptake

scholarly journals Stretch-stimulated glucose uptake in skeletal muscle is mediated by reactive oxygen species and p38 MAP-kinase

2009 ◽  
Vol 587 (13) ◽  
pp. 3363-3373 ◽  
Author(s):  
Melissa A. Chambers ◽  
Jennifer S. Moylan ◽  
Jeffrey D. Smith ◽  
Laurie J. Goodyear ◽  
Michael B. Reid
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Map Kinase ◽  
Glucose Uptake ◽  
Reactive Oxygen ◽  
P38 Map Kinase ◽  
Oxygen Species

scholarly journals Aldosterone Inhibits Insulin-Induced Glucose Uptake by Degradation of Insulin Receptor Substrate (IRS) 1 and IRS2 via a Reactive Oxygen Species-Mediated Pathway in 3T3-L1 Adipocytes

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1662-1669 ◽  
Author(s):  
Tsutomu Wada ◽  
Satoshi Ohshima ◽  
Eriko Fujisawa ◽  
Daisuke Koya ◽  
Hiroshi Tsuneki ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Glucocorticoid Receptor ◽  
Insulin Receptor ◽  
Receptor Antagonist ◽  
Glucose Uptake ◽  
Reactive Oxygen ◽  
Insulin Receptor Substrate ◽  
Oxygen Species ◽  
Metabolic Signaling

Serum aldosterone level is clinically known to correlate with body weight and insulin resistance. Because the underlying molecular mechanism is largely unknown, we examined the effect of aldosterone on insulin-induced metabolic signaling leading to glucose uptake in 3T3-L1 adipocytes. Aldosterone reduced the amounts of insulin receptor substrate (IRS) 1 and IRS2 in a time- and dose-dependent manner. As a result, insulin-induced phosphorylation of Akt-1 and -2, and subsequent uptake of 2-deoxyglucose were decreased. Degradation of IRSs was effectively prevented by a glucocorticoid receptor antagonist and antioxidant N-acetylcysteine, but not by a mineralocorticoid receptor antagonist. Because aldosterone induced phosphorylation of IRS1 at Ser307, responsible kinases were investigated, and we revealed that rapamycin and BMS345541, but neither SP600125 nor calphostin C, conferred for degradation of IRSs. Although lactacystin prevented the degradation of IRSs, glucose uptake was not preserved. Importantly, sucrose-gradient-sediment intracellular fraction analysis revealed that lactacystin did not effectively restore the reduction of IRS1 in the low-density microsome fraction, important for the transduction of insulin’s metabolic signaling. These results indicate that aldosterone deteriorates metabolic action of insulin by facilitating the degradation of IRS1 and IRS2 via glucocorticoid receptor-mediated production of reactive oxygen species, and activation of IκB Kinase β and target of rapamycin complex 1. Thus, aldosterone appears to be a novel key factor in the development of insulin resistance in visceral obesity.

scholarly journals Silica-coated magnetic-nanoparticle-induced cytotoxicity is reduced in microglia by glutathione and citrate identified using integrated omics

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Tae Hwan Shin ◽  
Balachandran Manavalan ◽  
Da Yeon Lee ◽  
Shaherin Basith ◽  
Chan Seo ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Reactive Oxygen Species ◽  
Tandem Mass Spectrometry ◽  
Glucose Uptake ◽  
Reactive Oxygen ◽  
Intracellular Reactive Oxygen Species ◽  
Tandem Mass ◽  
Oxygen Species ◽  
Chromatography Tandem Mass Spectrometry ◽  
The Brain

Abstract Background Nanoparticles have been utilized in brain research and therapeutics, including imaging, diagnosis, and drug delivery, owing to their versatile properties compared to bulk materials. However, exposure to nanoparticles leads to their accumulation in the brain, but drug development to counteract this nanotoxicity remains challenging. To date, concerns have risen about the potential toxicity to the brain associated with nanoparticles exposure via penetration of the brain blood barrier to address this issue. Methods Here the effect of silica-coated-magnetic nanoparticles containing the rhodamine B isothiocyanate dye [MNPs@SiO2(RITC)] were assessed on microglia through toxicological investigation, including biological analysis and integration of transcriptomics, proteomics, and metabolomics. MNPs@SiO2(RITC)-induced biological changes, such as morphology, generation of reactive oxygen species, intracellular accumulation of MNPs@SiO2(RITC) using transmission electron microscopy, and glucose uptake efficiency, were analyzed in BV2 murine microglial cells. Each omics data was collected via RNA-sequencing-based transcriptome analysis, liquid chromatography-tandem mass spectrometry-based proteome analysis, and gas chromatography- tandem mass spectrometry-based metabolome analysis. The three omics datasets were integrated and generated as a single network using a machine learning algorithm. Nineteen compounds were screened and predicted their effects on nanotoxicity within the triple-omics network. Results Intracellular reactive oxygen species production, an inflammatory response, and morphological activation of cells were greater, but glucose uptake was lower in MNPs@SiO2(RITC)-treated BV2 microglia and primary rat microglia in a dose-dependent manner. Expression of 121 genes (from 41,214 identified genes), and levels of 45 proteins (from 5918 identified proteins) and 17 metabolites (from 47 identified metabolites) related to the above phenomena changed in MNPs@SiO2(RITC)-treated microglia. A combination of glutathione and citrate attenuated nanotoxicity induced by MNPs@SiO2(RITC) and ten other nanoparticles in vitro and in the murine brain, protecting mostly the hippocampus and thalamus. Conclusions Combination of glutathione and citrate can be one of the candidates for nanotoxicity alleviating drug against MNPs@SiO2(RITC) induced detrimental effect, including elevation of intracellular reactive oxygen species level, activation of microglia, and reduction in glucose uptake efficiency. In addition, our findings indicate that an integrated triple omics approach provides useful and sensitive toxicological assessment for nanoparticles and screening of drug for nanotoxicity. Graphical Abstract

scholarly journals Modulation of Adipogenesis and Oxidative Status by Quercetin and Ochratoxin A: Positive or Negative Impact on Rat Adipocyte Metabolism?

Molecules ◽  
2019 ◽  
Vol 24 (20) ◽  
pp. 3726 ◽  
Author(s):  
Viktoria Dobrocsyova ◽  
Katarina Krskova ◽  
Marcela Capcarova ◽  
Stefan Zorad
Keyword(s):  
Reactive Oxygen Species ◽  
Adipose Tissue ◽  
Glucose Uptake ◽  
Ochratoxin A ◽  
Negative Impact ◽  
Adipogenic Differentiation ◽  
Reactive Oxygen ◽  
Oxidative Status ◽  
Ros Production ◽  
Oxygen Species

(1) Background: Impaired adipose tissue function leads to the development of metabolic disorders. Reactive oxygen species play a key role in the regulation of adipogenesis and insulin-stimulated glucose uptake by adipocytes. Quercetin (QCT) regulates adipogenesis by affecting the redox state of preadipocytes. Ochratoxin A (OTA) is one of the most prevalent mycotoxins contaminating food. It has cytotoxic, genotoxic, pro-inflammatory, and anti-adipogenic effects. Antioxidants are believed to protect cells from the cytotoxicity and genotoxicity induced by OTA. The aim of this study was to investigate the effect of QCT and OTA application on preadipocyte differentiation, oxidative status, and adipocyte metabolism. (2) Methods: Primary rat preadipocytes were isolated from subcutaneous adipose tissue of Wistar rats. Gene expressions were determined by qPCR. Cell viability, reactive oxygen species (ROS) production, glucose uptake, and lipid accumulation were determined using commercially available kits. (3) Results: A dose-dependent inhibitory effect of QCT on adipogenic differentiation was observed, which was accompanied by a decrease in ROS production. Reduced ROS formation is closely related to impaired glucose uptake by adipocytes. (4) Conclusions: The results of this study indicate a key role of ROS in regulating adipogenesis and metabolic pathways, which is affected by the application of QCT and/or OTA.

scholarly journals Allograft Inflammatory Factor-1 Mediates Macrophage-Induced Impairment of Insulin Signaling in Adipocytes

2018 ◽  
Vol 47 (1) ◽  
pp. 403-413 ◽  
Author(s):  
Jingqi Ren ◽  
Yaqiu Lin ◽  
Junni Tang ◽  
Hua Yue ◽  
Yanying Zhao
Keyword(s):  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Glucose Uptake ◽  
Insulin Signaling ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Inflammatory Factor ◽  
Oxygen Species ◽  
Intracellular Lipid ◽  
Species Production

Background/Aims: Allograft inflammatory factor-1 (AIF-1) is an inflammatory cytokine produced mainly by macrophages within human white adipose tissue. Its expression is increased in obese subjects and positively correlated with insulin resistance. The purpose of this study is to characterize the regulatory role of AIF-1 in insulin signaling of adipocyte. Methods: AIF-1 was over-expressed via transfection of AIF-1 cDNA into murine RAW 264.7 macrophages, and the constitutive expression of AIF-1 was decreased via transfection of targeting siRNA. Murine 3T3L1 adipocytes were treated with macrophage-conditioned medium or AIF-1 protein. Intracellular lipid accumulation was assayed by oil red O stain. Reactive oxygen species production was determinated by a flow cytometer and adipokine secretion was measured with ELISA. Glucose uptake was detected using the glucose oxidase method and insulin-signal-transduction related molecules were analyzed by Western blot. Results: Short term (48 h) AIF-1 treatment slightly promoted intracellular lipid storage in differentiating 3T3L1 cells. The protein stimulated reactive oxygen species production, provoked TNFα, IL6, resistin, but suppressed adiponectin release and insulin-stimulated glucose uptake both under normal basal and insulin resistance conditions. Furthermore, AIF-1 induced NF-κB activation, inhibited PPARγ expression, GLUT4 translocation to plasma membrane and Akt phosphorylation. Conclusion: Macrophage-derived AIF-1 up-regulated reactive oxygen species production, adipokine TNFα, IL6, resistin release, and inhibited adiponectin secretion. Moreover, it suppressed insulin-stimulated glucose uptake by down-regulating insulin signaling. Thus, AIF-1 could be related to obesity-related diseases.

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