title: Macrophage and adipocyte IGF1 maintain adipose tissue homeostasis during metabolic stresses.
abstract: OBJECTIVE
  Insulin-like growth factor-1 (IGF1) regulates differentiation and growth of tissues and reduces stress and injury. IGF1 also in a tissue-specific manner modulates the differentiation and lipid storage capacity of adipocytes in vitro, but its roles in adipose tissue development and response to stress are not known.
  
  
  METHODS
  To study IGF1 in vivo, the cellular sources of adipose tissue Igf1 expression were identified and mice were generated with targeted deletion in adipocytes and macrophages. The effects of adipocyte and macrophage deficiency of IGF1 on adipose tissue development and the response to chronic (high-fat feeding) and acute (cold challenge) stress were studied.
  
  
  RESULTS
  The expression of Igf1 by adipose tissue was derived from multiple cell types including adipocytes and macrophages. In lean animals, adipocytes were the primary source of IGF1, but in obesity expression by adipocytes was reduced and by macrophages increased, so as to maintain overall adipose tissue Igf1 expression. Genetic deletion studies revealed that adipocyte-derived IGF1 regulated perigonadal but not subcutaneous adipose tissue mass during high-fat feeding and the development of obesity. Conversely, macrophage-derived IGF1 acutely modulated perigonadal adipose tissue mass during thermogenic challenges.
  
  
  CONCLUSIONS
  Local IGF1 is not required in lean adipose tissue development but is required to maintain homeostasis during both chronic and acute metabolic stresses.
authors.affiliation: Department of Medicine, Naomi Berrie Diabetes Center, Columbia University, New York, New York, USA.
authors.forename: Hye Rim
authors.initials: HR
authors.lastname: Chang
authors.affiliation: Department of Medicine, Naomi Berrie Diabetes Center, Columbia University, New York, New York, USA.|Department of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon, Republic of Korea.
authors.forename: Hae Jin
authors.initials: HJ
authors.lastname: Kim
authors.affiliation: Department of Medicine, Naomi Berrie Diabetes Center, Columbia University, New York, New York, USA.
authors.forename: Xiaoyuan
authors.initials: X
authors.lastname: Xu
authors.affiliation: Department of Medicine, Naomi Berrie Diabetes Center, Columbia University, New York, New York, USA.
authors.forename: Anthony W
authors.initials: AW
authors.lastname: Ferrante
mesh_terms: D017667:Adipocytes / Q000378:metabolism* / Q000502:physiology*; D050156:Adipogenesis / Q000502:physiology; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D006706:Homeostasis / Q000502:physiology*; D007334:Insulin-Like Growth Factor I / Q000502:physiology*; D008264:Macrophages / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000503:physiopathology*; D013312:Stress, Physiological / Q000502:physiology*; D022722:Thermogenesis / Q000502:physiology
chemical_list: C519530:insulin-like growth factor-1, mouse; D007334:Insulin-Like Growth Factor I