Abstract：
:The molecular mechanisms of angiogenesis in relation to adipose tissue metabolism remain poorly understood. Here, we show that exposure of mice to cold led to activation of angiogenesis in both white and brown adipose tissues. In the inguinal depot, cold exposure resulted in elevated expression levels of brown-fat-associated proteins, including uncoupling protein-1 (UCP1) and PGC-1alpha. Proangiogenic factors such as VEGF were upregulated, and endogenous angiogenesis inhibitors, including thrombospondin, were downregulated. In wild-type mice, the adipose tissues became hypoxic during cold exposure; in UCP1(-/-) mice, hypoxia did not occur, but, remarkably, the augmented angiogenesis was unaltered and was thus hypoxia independent. Intriguingly, VEGFR2 blockage abolished the cold-induced angiogenesis and significantly impaired nonshivering thermogenesis capacity. Unexpectedly, VEGFR1 blockage resulted in the opposite effects: increased adipose vascularity and nonshivering thermogenesis capacity. Our findings have conceptual implications concerning application of angiogenesis modulators for treatment of obesity and metabolic disorders.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Xue Y,Petrovic N,Cao R,Larsson O,Lim S,Chen S,Feldmann HM,Liang Z,Zhu Z,Nedergaard J,Cannon B,Cao Ydoi
10.1016/j.cmet.2008.11.009subject
Has Abstractpub_date
2009-01-07 00:00:00pages
99-109issue
1eissn
1550-4131issn
1932-7420pii
S1550-4131(08)00361-6journal_volume
9pub_type
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