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  • Peris, EduardGothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology,University of Gothenburg (author)

Antioxidant treatment induces reductive stress associated with mitochondrial dysfunction in adipocytes

  • Article/chapterEnglish2019

Publisher, publication year, extent ...

  • 2019

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  • LIBRIS-ID:oai:gup.ub.gu.se/278335
  • https://gup.ub.gu.se/publication/278335URI
  • https://doi.org/10.1074/jbc.RA118.004253DOI
  • https://research.chalmers.se/publication/507547URI
  • https://research.chalmers.se/publication/508783URI

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  • Language:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

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  • beta-Adrenergic stimulation of adipose tissue increases mitochondrial density and activity (browning) that are associated with improved whole-body metabolism. Whereas chronically elevated levels of reactive oxygen species (ROS) in adipose tissue contribute to insulin resistance, transient ROS elevation stimulates physiological processes such as adipogenesis. Here, using a combination of biochemical and cell and molecular biology-based approaches, we studied whether ROS or antioxidant treatment affects beta 3-adrenergic receptor (beta 3-AR) stimulation-induced adipose tissue browning. We found that beta 3-AR stimulation increases ROS levels in cultured adipocytes, but, unexpectedly, pretreatment with different antioxidants (N-acetylcysteine, vitamin E, or GSH ethyl ester) did not prevent this ROS increase. Using fluorescent probes, we discovered that the antioxidant treatments instead enhanced beta 3-AR stimulation-induced mitochondrial ROS production. This pro-oxidant effect of antioxidants was, even in the absence of beta 3-AR stimulation, associated with decreased oxygen consumption and increased lactate production in adipocytes. We observed similar antioxidant effects in WT mice: N-acetylcysteine blunted beta 3-AR stimulation-induced browning of white adipose tissue and reduced mitochondrial activity in brown adipose tissue even in the absence of beta 3-AR stimulation. Furthermore, N-acetylcysteine increased the levels of peroxiredoxin 3 and superoxide dismutase 2 in adipose tissue, indicating increased mitochondrial oxidative stress. We interpret this negative impact of antioxidants on oxygen consumption in vitro and adipose tissue browning in vivo as essential adaptations that prevent a further increase in mitochondrial ROS production. In summary, these results suggest that chronic antioxidant supplementation can produce a paradoxical increase in oxidative stress associated with mitochondrial dysfunction in adipocytes.

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  • Micallef, Peter,1988Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology,University of Gothenburg(Swepub:gu)xmicpe (author)
  • Paul, Alexandra,1988Chalmers tekniska högskola,Chalmers University of Technology(Swepub:cth)apaul (author)
  • Palsdottir, Vilborg,1979Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology,University of Gothenburg(Swepub:gu)xpalvi (author)
  • Enejder, Annika,1969Chalmers tekniska högskola,Chalmers University of Technology(Swepub:cth)enejder (author)
  • Bauzá-Thorbrügge, MarcoGothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology,University of Gothenburg(Swepub:gu)xbauzm (author)
  • Olofsson, Charlotta S,1971Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology,University of Gothenburg(Swepub:gu)xoloch (author)
  • Wernstedt Asterholm, Ingrid,1978Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi,Institute of Neuroscience and Physiology, Department of Physiology,University of Gothenburg(Swepub:gu)xwerni (author)
  • Göteborgs universitetInstitutionen för neurovetenskap och fysiologi, sektionen för fysiologi (creator_code:org_t)

Related titles

  • In:Journal of Biological Chemistry294:7, s. 2340-23520021-92581083-351X

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