IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v6y2015i1d10.1038_ncomms8906.html
   My bibliography  Save this article

Selective enhancement of insulin sensitivity in the mature adipocyte is sufficient for systemic metabolic improvements

Author

Listed:
  • Thomas S. Morley

    (Touchstone Diabetes Center, The University of Texas Southwestern Medical Center)

  • Jonathan Y. Xia

    (Touchstone Diabetes Center, The University of Texas Southwestern Medical Center)

  • Philipp E. Scherer

    (Touchstone Diabetes Center, The University of Texas Southwestern Medical Center
    The University of Texas Southwestern Medical Center)

Abstract

Dysfunctional adipose tissue represents a hallmark of type 2 diabetes and systemic insulin resistance, characterized by fibrotic deposition of collagens and increased immune cell infiltration within the depots. Here we generate an inducible model of loss of function of the protein phosphatase and tensin homologue (PTEN), a phosphatase critically involved in turning off the insulin signal transduction cascade, to assess the role of enhanced insulin signalling specifically in mature adipocytes. These mice gain more weight on chow diet and short-term as well as long-term high-fat diet exposure. Despite the increase in weight, they retain enhanced insulin sensitivity, show improvements in oral glucose tolerance tests, display reduced adipose tissue inflammation and maintain elevated adiponectin levels. These improvements also lead to reduced hepatic steatosis and enhanced hepatic insulin sensitivity. Prolonging insulin action selectively in the mature adipocyte is therefore sufficient to maintain normal systemic metabolic homeostasis.

Suggested Citation

  • Thomas S. Morley & Jonathan Y. Xia & Philipp E. Scherer, 2015. "Selective enhancement of insulin sensitivity in the mature adipocyte is sufficient for systemic metabolic improvements," Nature Communications, Nature, vol. 6(1), pages 1-11, November.
  • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8906
    DOI: 10.1038/ncomms8906
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms8906
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/ncomms8906?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
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Vissarion Efthymiou & Lianggong Ding & Miroslav Balaz & Wenfei Sun & Lucia Balazova & Leon G. Straub & Hua Dong & Eric Simon & Adhideb Ghosh & Aliki Perdikari & Svenja Keller & Umesh Ghoshdastider & C, 2023. "Inhibition of AXL receptor tyrosine kinase enhances brown adipose tissue functionality in mice," Nature Communications, Nature, vol. 14(1), pages 1-22, December.

    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:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8906. 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.