title: Characteristics of adipose tissue macrophages and macrophage-derived insulin-like growth factor-1 in virus-induced obesity.
abstract: BACKGROUND
  Various pathogens are implicated in the induction of obesity. Previous studies have confirmed that human adenovirus 36 (Ad36) is associated with increased adiposity, improved glycemic control and induction of inflammation. The Ad36-induced inflammation is reflected in the infiltration of macrophages into adipose tissue. However, the characteristics and role of adipose tissue macrophages (ATMs) and macrophage-secreted factors in virus-induced obesity (VIO) are unclear. Although insulin-like growth factor-1 (IGF-1) is involved in obesity metabolism, the contribution of IGF secreted by macrophages in VIO has not been studied.
  
  
  METHODS
  Four-week-old male mice were studied 1 week and 12 weeks after Ad36 infection for determining the characteristics of ATMs in VIO and diet-induced obesity (DIO). In addition, macrophage-specific IGF-1-deficient (MIKO) mice were used to study the involvement of IGF-1 in VIO.
  
  
  RESULTS
  In the early stage of VIO (1 week after Ad36 infection), the M1 ATM sub-population increased, which increased the M1/M2 ratio, whereas DIO did not cause this change. In the late stage of VIO (12 weeks after Ad36 infection), the M1/M2 ratio did not change because the M1 and M2 ATM sub-populations increased to a similar extent, despite an increase in adiposity. By contrast, DIO increased the M1/M2 ratio. In addition, VIO in wild-type mice upregulated angiogenesis in adipose tissue and improved glycemic control. However, MIKO mice showed no increase in adiposity, angiogenesis, infiltration of macrophages into adipose tissue, or improvement in glycemic control after Ad36 infection.
  
  
  CONCLUSIONS
  These data suggest that IGF-1 secreted by macrophages may contribute to hyperplasia and hypertrophy in adipose tissue by increasing angiogenesis, which helps to maintain the 'adipose tissue robustness'.
authors.affiliation: Department of Biotechnology, The Catholic University of Korea, Bucheon-si, Republic of Korea.
authors.forename: S
authors.identifier: http://orcid.org/0000-0003-0759-7519
authors.initials: S
authors.lastname: Park
authors.affiliation: Department of Biotechnology, The Catholic University of Korea, Bucheon-si, Republic of Korea.
authors.forename: H-L
authors.initials: HL
authors.lastname: Park
authors.affiliation: Department of Biotechnology, The Catholic University of Korea, Bucheon-si, Republic of Korea.
authors.forename: S-Y
authors.initials: SY
authors.lastname: Lee
authors.affiliation: Department of Biotechnology, The Catholic University of Korea, Bucheon-si, Republic of Korea.
authors.forename: J-H
authors.initials: JH
authors.lastname: Nam
mesh_terms: D000256:Adenoviridae / Q000378:metabolism*; D000257:Adenoviridae Infections / Q000473:pathology*; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D004195:Disease Models, Animal; D006965:Hyperplasia / Q000473:pathology; D006984:Hypertrophy / Q000473:pathology; D007249:Inflammation / Q000473:pathology*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D008262:Macrophage Activation; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000378:metabolism / Q000473:pathology*
chemical_list: D007334:Insulin-Like Growth Factor I