VEGF-A - Expressing adipose tissue shows rapid beiging and enhanced survival after transplantation and confers IL-4-independent metabolic improvements

Jiyoung Park, Min Kim, Kai Sun, Yu Aaron An, Xue Gu, Philipp E. Scherer

Research output: Contribution to journalArticle

33 Scopus citations

Abstract

Adipocyte-derived vascular endothelial growth factor-A (VEGF-A) plays a crucial role in angiogenesis and contributes to adipocyte function and systemic metabolism, such as insulin resistance, chronic inflammation, and beiging of subcutaneous adipose tissue. Using a doxycyclineinducible adipocyte-specific VEGF-A - overexpressing mouse model, we investigated the dynamics of local VEGF-A effects on tissue beiging of adipose tissue transplants. VEGF-A overexpression in adipocytes triggers angiogenesis. We also observed a rapid appearance of beige fat cells in subcutaneous white adipose tissue as early as 2 days postinduction of VEGF-A. In contrast to conventional cold-induced beiging, VEGF-A - induced beiging is independent of interleukin-4. We subjected metabolically healthy VEGF-A - overexpressing adipose tissue to autologous transplantation. Transfer of subcutaneous adipose tissues taken from VEGF-A - overexpressing mice into diet-induced obese mice resulted in systemic metabolic benefits, associated with improved survival of adipocytes and a concomitant reduced inflammatory response. These effects of VEGF-A are tissue autonomous, inducing white adipose tissue beiging and angiogenesis within the transplanted tissue. Our findings indicate that manipulation of adipocyte functions with a bona fide angiogenic factor, such as VEGF-A, significantly improves the survival and volume retention of fat grafts and can convey metabolically favorable properties on the recipient on the basis of beiging.

Original languageEnglish (US)
Pages (from-to)1479-1490
Number of pages12
JournalDiabetes
Volume66
Issue number6
DOIs
StatePublished - Jun 1 2017

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

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