Increased angiogenesis protects against adipose hypoxia and fibrosis in metabolic disease-resistant 11β-hydroxysteroid dehydrogenase type 1 (HSD1)-deficient mice

J Biol Chem. 2012 Feb 3;287(6):4188-97. doi: 10.1074/jbc.M111.259325. Epub 2011 Dec 12.

Abstract

In obesity, rapidly expanding adipose tissue becomes hypoxic, precipitating inflammation, fibrosis, and insulin resistance. Compensatory angiogenesis may prevent these events. Mice lacking the intracellular glucocorticoid-amplifying enzyme 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1(-/-)) have "healthier" adipose tissue distribution and resist metabolic disease with diet-induced obesity. Here we show that adipose tissues of 11βHSD1(-/-) mice exhibit attenuated hypoxia, induction of hypoxia-inducible factor (HIF-1α) activation of the TGF-β/Smad3/α-smooth muscle actin (α-SMA) signaling pathway, and fibrogenesis despite similar fat accretion with diet-induced obesity. Moreover, augmented 11βHSD1(-/-) adipose tissue angiogenesis is associated with enhanced peroxisome proliferator-activated receptor γ (PPARγ)-inducible expression of the potent angiogenic factors VEGF-A, apelin, and angiopoietin-like protein 4. Improved adipose angiogenesis and reduced fibrosis provide a novel mechanism whereby suppression of intracellular glucocorticoid regeneration promotes safer fat expansion with weight gain.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 11-beta-Hydroxysteroid Dehydrogenase Type 1 / metabolism*
  • Actins / genetics
  • Actins / metabolism
  • Adipokines
  • Adipose Tissue / blood supply
  • Adipose Tissue / enzymology*
  • Adipose Tissue / pathology
  • Angiopoietin-Like Protein 4
  • Angiopoietins / genetics
  • Angiopoietins / metabolism
  • Animals
  • Apelin
  • Fibrosis / enzymology
  • Fibrosis / genetics
  • Fibrosis / physiopathology
  • Hypoxia / enzymology*
  • Hypoxia / pathology
  • Hypoxia / physiopathology
  • Hypoxia-Inducible Factor 1, alpha Subunit / genetics
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Insulin Resistance / genetics
  • Intercellular Signaling Peptides and Proteins / genetics
  • Intercellular Signaling Peptides and Proteins / metabolism
  • Male
  • Mice
  • Mice, Knockout
  • Neovascularization, Physiologic*
  • Obesity / enzymology*
  • Obesity / pathology
  • Obesity / physiopathology
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Signal Transduction*
  • Smad3 Protein / genetics
  • Smad3 Protein / metabolism
  • Transforming Growth Factor beta / genetics
  • Transforming Growth Factor beta / metabolism
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / metabolism
  • Weight Gain / genetics

Substances

  • Actins
  • Adipokines
  • Angiopoietin-Like Protein 4
  • Angiopoietins
  • Angptl4 protein, mouse
  • Apelin
  • Apln protein, mouse
  • Hif1a protein, mouse
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Intercellular Signaling Peptides and Proteins
  • PPAR gamma
  • Smad3 Protein
  • Smad3 protein, mouse
  • Transforming Growth Factor beta
  • Vascular Endothelial Growth Factor A
  • vascular endothelial growth factor A, mouse
  • 11-beta-Hydroxysteroid Dehydrogenase Type 1