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  • Medina-Gomez, GemaDepartment of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge/Addenbrooke’s Hospital, Cambridge, U.K (author)

The link between nutritional status and insulin sensitivity is dependent on the adipocyte-specific peroxisome proliferator-activated receptor-gamma2 isoform

  • Article/chapterEnglish2005

Publisher, publication year, extent ...

  • American Diabetes Association,2005
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:oru-70892
  • https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-70892URI
  • https://doi.org/10.2337/diabetes.54.6.1706DOI

Supplementary language notes

  • Language:English
  • Summary in:English

Part of subdatabase

Classification

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

Notes

  • The nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARgamma) is critically required for adipogenesis. PPARgamma exists as two isoforms, gamma1 and gamma2. PPARgamma2 is the more potent adipogenic isoform in vitro and is normally restricted to adipose tissues, where it is regulated more by nutritional state than PPARgamma1. To elucidate the relevance of the PPARgamma2 in vivo, we generated a mouse model in which the PPARgamma2 isoform was specifically disrupted. Despite similar weight, body composition, food intake, energy expenditure, and adipose tissue morphology, male mice lacking the gamma2 isoform were more insulin resistant than wild-type animals when fed a regular diet. These results indicate that insulin resistance associated with ablation of PPARgamma2 is not the result of lipodystrophy and suggests a specific role for PPARgamma2 in maintaining insulin sensitivity independently of its effects on adipogenesis. Furthermore, PPARgamma2 knockout mice fed a high-fat diet did not become more insulin resistant than those on a normal diet, despite a marked increase in their mean adipocyte cell size. These findings suggest that PPARgamma2 is required for the maintenance of normal insulin sensitivity in mice but also raises the intriguing notion that PPARgamma2 may be necessary for the adverse effects of a high-fat diet on carbohydrate metabolism.

Subject headings and genre

Added entries (persons, corporate bodies, meetings, titles ...)

  • Virtue, SamDepartment of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge/Addenbrooke’s Hospital, Cambridge, U.K (author)
  • Lelliott, ChristopherDepartment of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge/Addenbrooke’s Hospital, Cambridge, U.K (author)
  • Boiani, RominaInstitute of Normal Human Morphology, Faculty of Medicine, Ancona University, Ancona, Italy (author)
  • Campbell, MarkDepartment of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge/Addenbrooke’s Hospital, Cambridge, U.K (author)
  • Christodoulides, ConstantinosDepartment of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge/Addenbrooke’s Hospital, Cambridge, U.K (author)
  • Perrin, ChristopheCentre National de la Recherche Scientifique, Paul Sabatier University, Toulouse, France (author)
  • Jimenez-Linan, MercedesDepartment of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge/Addenbrooke’s Hospital, Cambridge, U.K (author)
  • Blount, MargaretDepartment of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge/Addenbrooke’s Hospital, Cambridge, U.K (author)
  • Dixon, JohnParadigm Therapeutics, Cambridge, U.K (author)
  • Zahn, DirkParadigm Therapeutics, Cambridge, U.K (author)
  • Thresher, Rosemary R.Paradigm Therapeutics, Cambridge, U.K (author)
  • Aparicio, SamParadigm Therapeutics, Cambridge, U.K (author)
  • Carlton, MarkParadigm Therapeutics, Cambridge, U.K (author)
  • Colledge, William H.Department of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge/Addenbrooke’s Hospital, Cambridge, U.K (author)
  • Kettunen, Mikko I.Department of Biochemistry, University of Cambridge, Cambridge, U.K. (author)
  • Seppänen-Laakso, TuulikkiVTT: Technical Research Centre of Finland, VTT Biotechnology, Espoo, Finland (author)
  • Sethi, Jaswinder K.Department of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge/Addenbrooke’s Hospital, Cambridge, U.K (author)
  • O'Rahilly, StephenDepartment of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge/Addenbrooke’s Hospital, Cambridge, U.K (author)
  • Brindle, KevinDepartment of Biochemistry, University of Cambridge, Cambridge, U.K. (author)
  • Cinti, SaverioInstitute of Normal Human Morphology, Faculty of Medicine, Ancona University, Ancona, Italy (author)
  • Oresic, Matej,1967-VTT: Technical Research Centre of Finland, VTT Biotechnology, Espoo, Finland(Swepub:oru)moc (author)
  • Burcelin, RemyCentre National de la Recherche Scientifique, Paul Sabatier University, Toulouse, France (author)
  • Vidal-Puig, AntonioDepartment of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge/Addenbrooke’s Hospital, Cambridge, U.K (author)
  • Department of Clinical Biochemistry, Histopathology, Physiology and Oncology, University of Cambridge/Addenbrooke’s Hospital, Cambridge, U.KInstitute of Normal Human Morphology, Faculty of Medicine, Ancona University, Ancona, Italy (creator_code:org_t)

Related titles

  • In:Diabetes: American Diabetes Association54:6, s. 1706-17160012-17971939-327X

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