PMID- 23011592
OWN - NLM
STAT- MEDLINE
DCOM- 20130125
LR  - 20211021
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Print)
IS  - 0012-1797 (Linking)
VI  - 61
IP  - 12
DP  - 2012 Dec
TI  - Neuropeptide Y1 receptor in immune cells regulates inflammation and insulin 
      resistance associated with diet-induced obesity.
PG  - 3228-38
LID - 10.2337/db12-0156 [doi]
AB  - Recruitment of activated immune cells into white adipose tissue (WAT) is linked 
      to the development of insulin resistance and obesity, but the mechanism behind 
      this is unclear. Here, we demonstrate that Y1 receptor signaling in immune cells 
      controls inflammation and insulin resistance in obesity. Selective deletion of Y1 
      receptors in the hematopoietic compartment of mice leads to insulin resistance 
      and inflammation in WAT under high fat-fed conditions. This is accompanied by 
      decreased mRNA expression of the anti-inflammatory marker adiponectin in WAT and 
      an increase of the proinflammatory monocyte chemoattractant protein-1 (MCP-1). In 
      vitro, activated Y1-deficient intraperitoneal macrophages display an increased 
      inflammatory response, with exacerbated secretion of MCP-1 and tumor necrosis 
      factor, whereas addition of neuropeptide Y to wild-type macrophages attenuates 
      the release of these cytokines, this effect being blocked by Y1 but not Y2 
      receptor antagonism. Importantly, treatment of adipocytes with the supernatant of 
      activated Y1-deficient macrophages causes insulin resistance, as demonstrated by 
      decreased insulin-induced phosphorylation of the insulin receptor and Akt as well 
      as decreased expression of insulin receptor substrate 1. Thus, Y1 signaling in 
      hematopoietic-derived cells such as macrophages is critical for the control of 
      inflammation and insulin resistance in obesity.
FAU - Macia, Laurence
AU  - Macia L
AD  - Neuroscience Research Program, Garvan Institute of Medical Research, 
      Darlinghurst, New South Wales, Australia.
FAU - Yulyaningsih, Ernie
AU  - Yulyaningsih E
FAU - Pangon, Laurent
AU  - Pangon L
FAU - Nguyen, Amy D
AU  - Nguyen AD
FAU - Lin, Shu
AU  - Lin S
FAU - Shi, Yan C
AU  - Shi YC
FAU - Zhang, Lei
AU  - Zhang L
FAU - Bijker, Martijn
AU  - Bijker M
FAU - Grey, Shane
AU  - Grey S
FAU - Mackay, Fabienne
AU  - Mackay F
FAU - Herzog, Herbert
AU  - Herzog H
FAU - Sainsbury, Amanda
AU  - Sainsbury A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120925
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Chemokine CCL2)
RN  - 0 (Dietary Fats)
RN  - 0 (Receptors, Neuropeptide Y)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (neuropeptide Y-Y1 receptor)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Animals
MH  - Cell Differentiation
MH  - Chemokine CCL2/genetics/metabolism
MH  - Dietary Fats/adverse effects
MH  - Eating/genetics/physiology
MH  - Female
MH  - Genotype
MH  - Inflammation/genetics/immunology/*metabolism
MH  - Insulin Resistance/genetics/*physiology
MH  - Mice
MH  - Mice, Knockout
MH  - Obesity/etiology/*immunology/*metabolism
MH  - Polymerase Chain Reaction
MH  - Receptors, Neuropeptide Y/genetics/*metabolism
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
PMC - PMC3501846
EDAT- 2012/09/27 06:00
MHDA- 2013/01/26 06:00
PMCR- 2013/12/01
CRDT- 2012/09/27 06:00
PHST- 2012/09/27 06:00 [entrez]
PHST- 2012/09/27 06:00 [pubmed]
PHST- 2013/01/26 06:00 [medline]
PHST- 2013/12/01 00:00 [pmc-release]
AID - db12-0156 [pii]
AID - 0156 [pii]
AID - 10.2337/db12-0156 [doi]
PST - ppublish
SO  - Diabetes. 2012 Dec;61(12):3228-38. doi: 10.2337/db12-0156. Epub 2012 Sep 25.