CORDIS
EU research results

CORDIS

English EN
New mechanisms of angiogenesis modulators in switching between white and brown adipose tissues

New mechanisms of angiogenesis modulators in switching between white and brown adipose tissues

Objective

Understanding the molecular mechanisms underlying adipose blood vessel growth or regression opens new fundamentally insight into novel therapeutic options for the treatment of obesity and its related metabolic diseases such as type 2 diabetes and cancer. Unlike any other tissues in the body, the adipose tissue constantly experiences expansion and shrinkage throughout the adult life. Adipocytes in the white adipose tissue have the ability to switch into metabolically highly active brown-like adipocytes. Brown adipose tissue (BAT) contains significantly higher numbers of microvessels than white adipose tissue (WAT) in order to adopt the high rates of metabolism. Thus, an angiogenic phenotype has to be switched on during the transition from WAT into BAT. We have found that acclimation of mice in cold could induce transition from inguinal and epidedymal WAT into BAT by upregulation of angiogenic factor expression and down-regulations of angiogenesis inhibitors (Xue et al, Cell Metabolism, 2009). The transition from WAT into BAT is dependent on vascular endothelial growth factor (VEGF) that primarily targets on vascular endothelial cells via a tissue hypoxia-independent mechanism. VEGF blockade significantly alters adipose tissue metabolism. In another genetic model, we show similar findings that angiogenesis is crucial to mediate the transition from WAT into BAT (Xue et al, PNAS, 2008). Here we propose that the vascular tone determines the metabolic switch between WAT and BAT. Characterization of these novel angiogenic pathways may reveal new mechanisms underlying development of obesity- and metabolism-related disease complications and may define novel therapeutic targets. Thus, the benefit of this research proposal is enormous and is aimed to treat the most common and highly risk human health conditions in the modern time.
Leaflet | Map data © OpenStreetMap contributors, Credit: EC-GISCO, © EuroGeographics for the administrative boundaries

Principal Investigator

Yihai Cao (Prof.)

Host institution

KAROLINSKA INSTITUTET

Address

Nobels Vag 5
17177 Stockholm

Sweden

Activity type

Higher or Secondary Education Establishments

EU Contribution

€ 2 411 547

Principal Investigator

Yihai Cao (Prof.)

Administrative Contact

Marlene Brink-Sinervo (Ms.)

Beneficiaries (1)

Sort alphabetically

Sort by EU Contribution

Expand all

KAROLINSKA INSTITUTET

Sweden

EU Contribution

€ 2 411 547

Project information

Grant agreement ID: 250021

Status

Closed project

  • Start date

    1 March 2010

  • End date

    28 February 2015

Funded under:

FP7-IDEAS-ERC

  • Overall budget:

    € 2 411 547

  • EU contribution

    € 2 411 547

Hosted by:

KAROLINSKA INSTITUTET

Sweden