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  • Hogh, K-Lynn N.Northern Medical Program, University of Northern British Columbia, Prince George BC, Canada (författare)

Overexpression of PPARγ specifically in pancreatic β-cells exacerbates obesity-induced glucose intolerance, reduces β-cell mass, and alters islet lipid metabolism in male mice

  • Artikel/kapitelEngelska2014

Förlag, utgivningsår, omfång ...

  • Oxford University Press,2014
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:oru-63696
  • https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-63696URI
  • https://doi.org/10.1210/en.2014-1076DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Funding agencies:Canadian Diabetes Association  University of Northern British Columbia Research Project Awards  
  • The contribution of peroxisomal proliferator-activated receptor (PPAR)-γ agonism in pancreatic β-cells to the antidiabetic actions of thiazolidinediones has not been clearly elucidated. Genetic models of pancreatic β-cell PPARγ ablation have revealed a potential role for PPARγ in β-cell expansion in obesity but a limited role in normal β-cell physiology. Here we overexpressed PPARγ1 or PPARγ2 specifically in pancreatic β-cells of mice subjected to high-fat feeding using an associated adenovirus (β-PPARγ1-HFD and β-PPARγ2-HFD mice). We show β-cell-specific PPARγ1 or PPARγ2 overexpression in diet-induced obese mice exacerbated obesity-induced glucose intolerance with decreased β-cell mass, increased islet cell apoptosis, and decreased plasma insulin compared with obese control mice (β-eGFP-HFD mice). Analysis of islet lipid composition in β-PPARγ2-HFD mice revealed no significant changes in islet triglyceride content and an increase in only one of eight ceramide species measured. Interestingly β-PPARγ2-HFD islets had significantly lower levels of lysophosphatidylcholines, lipid species shown to enhance insulin secretion in β-cells. Gene expression profiling revealed increased expression of uncoupling protein 2 and genes involved in fatty acid transport and β-oxidation. In summary, transgenic overexpression of PPARγ in β-cells in diet-induced obesity negatively impacts whole-animal carbohydrate metabolism associated with altered islet lipid content, increased expression of β-oxidative genes, and reduced β-cell mass.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Craig, Michael N.Northern Medical Program, University of Northern British Columbia, Prince George BC, Canada (författare)
  • Uy, Christopher E.Northern Medical Program, University of Northern British Columbia, Prince George BC, Canada (författare)
  • Nygren, HeliVTT Technical Research Centre of Finland, Espoo, Finland; Steno Diabetes Center A/S, Gentofte, Denmark (författare)
  • Asadi, AliDepartment of Cellular and Physiological Sciences and Faculty of Medicine, University of British Columbia, Vancouver BC, Canada (författare)
  • Speck, MadelineChild and Family Research Institute, Vancouver BC, Canada (författare)
  • Fraser, Jordie D. (författare)
  • Rudecki, Alexander P.Northern Medical Program, University of Northern British Columbia, Prince George BC, Canada (författare)
  • Baker, Robert K.Department of Cellular and Physiological Sciences and Faculty of Medicine, University of British Columbia, Vancouver BC, Canada (författare)
  • Oresic, Matej,1967-Örebro universitet,Institutionen för medicinska vetenskaper,VTT Technical Research Centre of Finland, Espoo, Finland; Steno Diabetes Center A/S, Gentofte, Denmark(Swepub:oru)moc (författare)
  • Gray, Sarah L.Northern Medical Program, University of Northern British Columbia, Prince George BC, Canada (författare)
  • Northern Medical Program, University of Northern British Columbia, Prince George BC, CanadaVTT Technical Research Centre of Finland, Espoo, Finland; Steno Diabetes Center A/S, Gentofte, Denmark (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Endocrinology: Oxford University Press155:10, s. 3843-38520013-72271945-7170

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