title: Macrophage-colony stimulating factor in obese adipose tissue: studies with heterozygous op/+ mice.
abstract: OBJECTIVE
  We examined the gene expression of macrophage-colony stimulating factor (M-CSF) in mice with diet-induced obesity and in genetically obese mice. We also examined the effect of decreased M-CSF signaling on the susceptibility to obesity and macrophage recruitment into the adipose tissue of mice.
  
  
  METHODS
  The adipose tissue from mice with diet-induced obesity, obese KKA(y) mice, and ob/ob obese mice was used for RNA preparation. Production of M-CSF and monocyte chemoattractant protein-1 (MCP-1) was examined by quantitative real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay. The op/+ heterozygous mice, with decreased functional M-CSF expression, were placed on a high-fat diet or crossed with KKA(y) mice to study the susceptibility to obesity. The gene expression of macrophage markers in adipose tissue was examined.
  
  
  RESULTS
  The expression of M-CSF was not significantly changed in mice on a high-fat diet or in either type of genetic obesity (KKA(y) or ob/ob mice). No change in the degree of obesity or macrophage-related gene expression (F4/80, CD68, and MCP-1) in the adipose tissue was observed in op/+ mice compared with +/+ control mice, which were either treated with a high-fat diet or crossed with KKA(y) mice.
  
  
  CONCLUSIONS
  This study demonstrated that there was no significant change in the expression of M-CSF in the adipose tissue from obese mice and only a minor phenotypic change, such as macrophage infiltration, in the adipose tissue from op/+ mice, suggesting that M-CSF does not play a major role in macrophage recruitment in the adipose tissue of obese mice.
authors: Department of Molecular Medicine and Metabolism, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10 Kanda-surugadai, Tokyo 101-0062, Japan.
authors: Satoshi
authors: S
authors: Sugita
authors: Yasutomi
authors: Y
authors: Kamei
authors: Jun-Ichiro
authors: J
authors: Oka
authors: Takayoshi
authors: T
authors: Suganami
authors: Yoshihiro
authors: Y
authors: Ogawa
mesh_terms: D000818:Animals; D000943:Antigens, Differentiation / Q000096:biosynthesis / Q000235:genetics; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000235:genetics; D003433:Crosses, Genetic; D006651:Histocytochemistry; D016173:Macrophage Colony-Stimulating Factor / Q000096:biosynthesis* / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D009765:Obesity / Q000235:genetics / Q000276:immunology*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D016186:Receptor, Macrophage Colony-Stimulating Factor / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050151:Subcutaneous Fat / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics
chemical_list: D000943:Antigens, Differentiation; D018932:Chemokine CCL2; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; C036763:monocyte-macrophage differentiation antigen; D016173:Macrophage Colony-Stimulating Factor; D016186:Receptor, Macrophage Colony-Stimulating Factor