PMID- 23420608
OWN - NLM
STAT- MEDLINE
DCOM- 20140128
LR  - 20190720
IS  - 1347-5215 (Electronic)
IS  - 0918-6158 (Linking)
VI  - 36
IP  - 5
DP  - 2013
TI  - Infiltration of M1 macrophages into adipose tissue of ddY-H mice preceding 
      spontaneous appearances of insulin resistance.
PG  - 825-32
AB  - We have isolated insulin resistant mice (ddY-H mice) which are spontaneously 
      induced at 12-weeks of age even if fed with the standard chow pellets. Since 
      accumulated evidences have suggested that an appearance of insulin resistance is 
      associated with obesity and a state of inflammation in adipose tissue, the 
      present study investigated an appearance of macrophages in adipose tissue of 
      ddY-H mice. Although ddY-H mice were fed the standard chow pellets ad libitam, 
      increases in body weight, adipose tissue mass, and fat cell size were observed. 
      In adipose tissues of ddY-H mice, gene expression of monocyte chemoattractant 
      protein-1 (MCP-1) elevated slightly at 5-weeks of age and was maintained at 
      higher levels at 9- and 12-weeks of age, and MCP-1 content in adipose tissue 
      increased 2-fold at 12-weeks of age. Also, increased gene expressions of CD68 and 
      F4/80, markers of macrophage, in adipose tissue were observed at 9-weeks of age. 
      In addition, F4/80 positive cells were histologically found in adipose tissue at 
      15-weeks of age but not at 7-weeks of age, suggesting an increased infiltration 
      of macrophage into adipose tissue. In adipose tissue of ddY-H mice, gene 
      expressions of CD11c and toll-like receptor 4 (TLR4), markers of proinflammatory 
      macrophages (M1), markedly increased although those of CD163 and mannose receptor 
      (MR), markers of anti-inflammatory macrophages (M2), did not change. These 
      results suggest that proinflammatory (M1) macrophages infiltrate into enlarged 
      adipose tissues of ddY-H mice, which is preceding spontaneous appearance of 
      insulin resistance.
FAU - Maeda, Toshio
AU  - Maeda T
AD  - Department of Clinical Pharmaceutics & Pharmacy Practice, Graduate School of 
      Pharmaceutical Sciences, University of Shizuoka, Shizuoka 422-8526, Japan. 
      maeda@u-shizuoka-ken.ac.jp
FAU - Noge, Ichiro
AU  - Noge I
FAU - Kagawa, Yoshiyuki
AU  - Kagawa Y
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20130218
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Adipose Tissue/anatomy & histology/cytology/*physiology
MH  - Animals
MH  - Body Weight
MH  - Cell Size
MH  - Chemokine CCL2/genetics
MH  - *Disease Models, Animal
MH  - Gene Expression
MH  - Insulin Resistance/*physiology
MH  - Macrophages/*physiology
MH  - Male
MH  - Mice
EDAT- 2013/02/20 06:00
MHDA- 2014/01/29 06:00
CRDT- 2013/02/20 06:00
PHST- 2013/02/20 06:00 [entrez]
PHST- 2013/02/20 06:00 [pubmed]
PHST- 2014/01/29 06:00 [medline]
AID - DN/JST.JSTAGE/bpb/b12-01014 [pii]
AID - 10.1248/bpb.b12-01014 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 2013;36(5):825-32. doi: 10.1248/bpb.b12-01014. Epub 2013 Feb 18.