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Remodeling of human adipose tissue to metabolically favorable profile requires PI3K activation.
Author(s) -
Rogers Pamela M,
Mashtalir Nazar,
Dhurandhar Nikhil V
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1052-c
Subject(s) - adipose tissue , adipogenesis , adipocyte , wortmannin , adiponectin , angiogenesis , medicine , endocrinology , adipose tissue macrophages , biology , inflammation , kinase , white adipose tissue , insulin resistance , pi3k/akt/mtor pathway , cancer research , microbiology and biotechnology , insulin , signal transduction
Previously, we showed that experimental infection of rodents with a human adenovirus, Ad‐36, results in insulin sensitivity and increased adiposity. In vitro Ad‐36 infection of human adipocyte progenitors up‐regulates PI3 Kinase signaling pathway, and increases differentiation and lipid accumulation. We investigated the ability of Ad‐36 to remodel adipose tissue via PI3 Kinase activation by infecting human adipose tissue explants in the presence or absence of Wortmannin (WM), a well‐characterized PI3 Kinase inhibitor. We assessed adipose tissue remodeling by measuring markers for adiposity (PPARγ2, aP2), angiogenesis (PECAM‐1), insulin sensitivity (adiponectin, FAS), and inflammation (MCP‐1). Collectively, these results suggest that Ad‐36 remodels human adipose tissue to exhibit greater adipogenesis, angiogenesis, insulin sensitivity and favorable inflammatory cytokine profile, which requires PI3 Kinase activity. Potential of Ad‐36 to remodel adipose tissue may provide therapeutic targets for remodeling unfavorable adipose tissue profile common in obesity, diabetes and metabolic syndrome. Funded by NIH R‐01 DK066164. Fold change in gene expression by qRT‐PCR (p< .05). Ad‐36 group is compared to uninfected control. (Ad‐36 + WM) group is compared to Ad‐36 alone.