IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v403y2000i6772d10.1038_35002663.html
   My bibliography  Save this article

Leptin and diabetes in lipoatrophic mice

Author

Listed:
  • Oksana Gavrilova

    (Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health)

  • Bernice Marcus-Samuels

    (Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health)

  • Lisa R. Leon

    (Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health)

  • Charles Vinson

    (Laboratory of Metabolism, National Cancer Institute, National Institutes of Health)

  • Marc L. Reitman

    (Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health)

Abstract

Lipoatrophic (lipodystrophic) diabetes is a disorder in which insulin resistance and hyperglycaemia are associated with a reduced body-fat mass1, in contrast to the usual association of diabetes with obesity. Transgenic mice with differing degrees of fat loss can be used as models for lipoatrophy2,3,4. Using the aP2-SREBP-1c mouse3, which has a moderate fat deficiency, Shimomura et al. showed that leptin treatment reverses the diabetes, concluding that insulin resistance in congenital generalized lipodystrophy can be explained by a leptin deficiency5. However, we have used a more severe model of lipoatrophy, the A-ZIP/F-1 mouse2,6, in which we find that leptin treatment is only slightly effective in correcting diabetes.

Suggested Citation

  • Oksana Gavrilova & Bernice Marcus-Samuels & Lisa R. Leon & Charles Vinson & Marc L. Reitman, 2000. "Leptin and diabetes in lipoatrophic mice," Nature, Nature, vol. 403(6772), pages 850-850, February.
    • Handle: RePEc:nat:nature:v:403:y:2000:i:6772:d:10.1038_35002663
    DOI: 10.1038/35002663
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/35002663
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.
    File URL: https://libkey.io/10.1038/35002663?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:nature:v:403:y:2000:i:6772:d:10.1038_35002663. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.