PMID- 22396205
OWN - NLM
STAT- MEDLINE
DCOM- 20120725
LR  - 20220409
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Print)
IS  - 0012-1797 (Linking)
VI  - 61
IP  - 6
DP  - 2012 Jun
TI  - Stress augments insulin resistance and prothrombotic state: role of visceral 
      adipose-derived monocyte chemoattractant protein-1.
PG  - 1552-61
LID - 10.2337/db11-0828 [doi]
AB  - Stressors contribute to thrombosis and insulin resistance. Since obesity-related 
      adipose inflammation is also involved in these pathological states, we assumed 
      that stress correlates with adipose inflammation. Male mice were subjected to 
      2-week intermittent restraint stress. Expression of plasma lipids, 
      monocyte/macrophage markers (CD11b, CD68, and F4/80), proinflammatory cytokines 
      (monocyte chemoattractant protein-1 [MCP-1], tumor necrosis factor-alpha, and 
      interleukin-6), adiponectin, heat shock protein 70.1 (HSP70.1), and coagulation 
      factors (plasminogen activation inhibitor-1 [PAI-1] and tissue factor [TF]) in 
      blood and inguinal white adipose tissue (WAT) was determined using 
      immunohistochemistry, enzyme-linked immunosorbent assay, and RT-PCR, 
      respectively. Glucose metabolism was assessed by glucose tolerance tests (GTTs) 
      and insulin tolerance tests, and expression of insulin receptor substrate-1 
      (IRS-1) and glucose transporter 4 (GLUT4) in WAT. To examine effects of MCP-1 
      blockade, animals were treated with control or neutralizing antibody, or 
      transplanted with control or 7ND (dominant-negative form of MCP-1)-overexpressing 
      adipose-derived stromal cells (ADSCs). Stress increased monocyte accumulation, 
      free fatty acids, proinflammatory cytokine, and HSP70.1 and reduced adiponectin. 
      Adipose stromal cells highly expressed MCP-1. The stress-induced adipose 
      inflammation increased PAI-1 and TF but did not give rise to thrombus formation. 
      Without any changes in GTT, stress worsened insulin sensitivity and decreased 
      IRS-1 and GLUT4 in WAT. Neutralizing antibody and 7ND-ADSCs reversed 
      stress-induced adipose inflammation, procoagulant state, and insulin resistance. 
      Stress evoked adipose inflammation to increase coagulation factors and impair 
      insulin sensitivity through adipose-derived MCP-1.
FAU - Uchida, Yasuhiro
AU  - Uchida Y
AD  - Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, 
      Japan.
FAU - Takeshita, Kyosuke
AU  - Takeshita K
FAU - Yamamoto, Koji
AU  - Yamamoto K
FAU - Kikuchi, Ryosuke
AU  - Kikuchi R
FAU - Nakayama, Takayuki
AU  - Nakayama T
FAU - Nomura, Mieko
AU  - Nomura M
FAU - Cheng, Xian Wu
AU  - Cheng XW
FAU - Egashira, Kensuke
AU  - Egashira K
FAU - Matsushita, Tadashi
AU  - Matsushita T
FAU - Nakamura, Hideo
AU  - Nakamura H
FAU - Murohara, Toyoaki
AU  - Murohara T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120306
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Antibodies, Neutralizing)
RN  - 0 (Blood Glucose)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Glucose Transporter Type 4)
RN  - 0 (Insulin Receptor Substrate Proteins)
RN  - 0 (Irs1 protein, mouse)
RN  - 0 (Plasminogen Activator Inhibitor 1)
SB  - IM
MH  - Adipose Tissue/*metabolism
MH  - Animals
MH  - Antibodies, Neutralizing
MH  - Blood Glucose/metabolism
MH  - Chemokine CCL2/*metabolism
MH  - Cytokines/blood
MH  - Glucose Tolerance Test
MH  - Glucose Transporter Type 4/metabolism
MH  - Inflammation/metabolism
MH  - Insulin Receptor Substrate Proteins/metabolism
MH  - Insulin Resistance/*physiology
MH  - Male
MH  - Mice
MH  - Monocytes/*metabolism
MH  - Plasminogen Activator Inhibitor 1/metabolism
MH  - Stress, Physiological/*physiology
PMC - PMC3357288
EDAT- 2012/03/08 06:00
MHDA- 2012/07/26 06:00
PMCR- 2013/06/01
CRDT- 2012/03/08 06:00
PHST- 2012/03/08 06:00 [entrez]
PHST- 2012/03/08 06:00 [pubmed]
PHST- 2012/07/26 06:00 [medline]
PHST- 2013/06/01 00:00 [pmc-release]
AID - db11-0828 [pii]
AID - 0828 [pii]
AID - 10.2337/db11-0828 [doi]
PST - ppublish
SO  - Diabetes. 2012 Jun;61(6):1552-61. doi: 10.2337/db11-0828. Epub 2012 Mar 6.