PMID- 18268047
OWN - NLM
STAT- MEDLINE
DCOM- 20080804
LR  - 20090220
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
VI  - 57
IP  - 5
DP  - 2008 May
TI  - Monocyte chemoattractant protein deficiency fails to restrain macrophage 
      infiltration into adipose tissue [corrected].
PG  - 1254-61
LID - 10.2337/db07-1061 [doi]
AB  - OBJECTIVE: Monocyte chemoattractant protein-1 (MCP-1), a CC-motif chemokine, has 
      been proposed to play critical roles in insulin resistance and recruitment of 
      monocytes into adipose tissue. We hypothesized that the absence of MCP-1 would 
      improve the former and diminish the latter. RESEARCH DESIGN AND METHODS: We 
      investigated these two hypotheses by quantifying glucose metabolism and the 
      accumulation of macrophages in adipose tissue of control and MCP-1-deficient 
      (Mcp1(-)(/)(-)) mice after feeding the animals a high-fat diet for 10 or 16 
      weeks. RESULTS: We first established that the two strains were in the same 
      genetic background and that macrophage recruitment into inflamed peritoneum was 
      markedly reduced in the MCP-1-deficient animals. In striking contrast, 
      independent studies at two different facilities at either an early or late time 
      point failed to detect any impairment in macrophage accumulation in adipose 
      tissue of fat-fed Mcp1(-/-) mice. Immunoblot analysis revealed higher levels of 
      Mac2, a macrophage-specific protein, in multiple fat depots of Mcp1(-/-) mice fed 
      a high-fat diet. These mice also had significantly more adipose tissue than 
      control mice, but their glucose metabolism was similar. CONCLUSIONS: Our 
      observations suggest that MCP-1 does not play a prominent a role in promoting 
      macrophage recruitment into adipose tissue or in systemic insulin resistance.
FAU - Kirk, Elizabeth A
AU  - Kirk EA
AD  - Nutritional Sciences Program, Department of Pathobiology, University of 
      Washington, Seattle, Washington 98195, USA. eakirk@u.washington.edu
FAU - Sagawa, Zachary K
AU  - Sagawa ZK
FAU - McDonald, Thomas O
AU  - McDonald TO
FAU - O'Brien, Kevin D
AU  - O'Brien KD
FAU - Heinecke, Jay W
AU  - Heinecke JW
LA  - eng
GR  - HL-030086/HL/NHLBI NIH HHS/United States
GR  - HL-078527/HL/NHLBI NIH HHS/United States
GR  - HL-086798/HL/NHLBI NIH HHS/United States
GR  - P30-DK-017047/DK/NIDDK NIH HHS/United States
GR  - P50-ES-07083/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20080211
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Blood Glucose)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Dietary Fats)
RN  - 0 (Triglycerides)
SB  - IM
EIN - Diabetes. 2008 Sep;57(9):2252
MH  - Adipose Tissue/*physiology
MH  - Animal Feed
MH  - Animals
MH  - Blood Glucose/metabolism
MH  - Chemokine CCL2/deficiency/genetics/*physiology
MH  - Diet, Fat-Restricted
MH  - Dietary Fats
MH  - Humans
MH  - Insulin Resistance/physiology
MH  - Macrophages, Peritoneal/*physiology
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Reference Values
MH  - Triglycerides/blood
EDAT- 2008/02/13 09:00
MHDA- 2008/08/05 09:00
CRDT- 2008/02/13 09:00
PHST- 2008/02/13 09:00 [pubmed]
PHST- 2008/08/05 09:00 [medline]
PHST- 2008/02/13 09:00 [entrez]
AID - db07-1061 [pii]
AID - 10.2337/db07-1061 [doi]
PST - ppublish
SO  - Diabetes. 2008 May;57(5):1254-61. doi: 10.2337/db07-1061. Epub 2008 Feb 11.