Skip NavigationSkip to Content
Return Return to Search Results

A model for obesity and gigantism due to disruption of the Ankrd26 gene

  1. Author:
    Bera, T. K.
    Liu, X. F.
    Yamada, M.
    Gavrilovat, O.
    Mezey, E.
    Tessarollo, L.
    Anver, M.
    Hahn, Y.
    Lee, B.
    Pastan, I.

  2. Author Address

    Bera, Tapan K.; Liu, Xiu-Fen, Yamada, Masanori, Hahn, Yoonsoo, Lee, Byungkook, Pastan, Ira] NCI, Mol Biol Lab, NIH, Ctr Canc Res, Bethesda, MD 20892 USA. [Gavrilovat, Oksana] NIDDK, Mouse Metab Core Lab, Natl Inst Hlth, Bethesda, MD 20892 USA. [Mezey, Eva] Natl Inst Dent & Craniofacial Res, Craniofacial & Skeleta Dis Branch, Natl Inst Hlth, Bethesda, MD 20892 USA. [Tessarollo, Lino] NCI, Mouse Canc Genet Program, Canc Res Ctr, Frederick, MD 21702 USA. [Anver, Miriam] NCI, SAIC Frederick, Pathol Histotechnol Lab, Frederick, MD 21702 USA.
    1. Year: 2008
  2. Journal: Proceedings of the National Academy of Sciences of the United States of America
    1. 105
    2. 1
    3. Pages: 270-275
  4. Type of Article: Article
  1. Abstract:

    Obesity is a major health hazard that is caused by a combination of genetic and behavioral factors. Several models of obesity have been described in mice that have defects in the production of peptide hormones, in the function of cell membrane receptors, or in a transcription factor required for neuronal cell development. We have been investigating the function of a family of genes(POTE and ANKRD26) that encode proteins that are associated with the inner aspect of the cell membrane and that contain both ankyrin repeats and spectrin helices, motifs known to interact with signaling proteins in the cell. To assess the function of ANKRD26, we prepared a mutant mouse with partial inactivation of the Ankrd26 gene. We find that the homozygous mutant mice develop extreme obesity, insulin resistance, and an increase in body size. The obesity is associated with hyperphagia with no reduction in energy expenditure and activity. The Ankrd26 protein is expressed in the arcuate and ventromedial nuclei within the hypothalamus and in the ependyma and the circumventricular organs that act as an interface between the peripheral circulation and the brain. In the enlarged hearts of the mutant mice, the levels of both phospho-Akt and mTOR were elevated. These results show that alterations in an unidentified gene can lead to obesity and identify a molecular target for the treatment of obesity.

    See More

  1. Keywords:

External Sources

  1. PMID: 18162531

Library Notes

  1. No notes added.
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel