PMID- 26155140
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150709
LR  - 20200930
IS  - 1426-3912 (Print)
IS  - 1644-4124 (Electronic)
IS  - 1426-3912 (Linking)
VI  - 39
IP  - 3
DP  - 2014
TI  - Diet-induced obesity mediates a proinflammatory response in pancreatic beta cell via 
      toll-like receptor 4.
PG  - 306-15
LID - 10.5114/ceji.2014.45940 [doi]
AB  - Toll-like receptor 4 has an important role in inflammation and immunity. Whether 
      TLR4 signaling contributes to the link between insulin resistance and islet beta 
      cell dysfunction is an unanswered question. Here, we show that in the face of the 
      same high-fat continuous stimulation for 24 weeks, in TLR4-/- HF mice, the 
      weight, fraction of the liver, epididymal fat pad fraction, as well as blood 
      glucose and insulin levels were lower than in the WT HF group. In TLR4-/- HF 
      mice, the O2 consumption, CO2 production and activities were higher than in the 
      WT HF group. Glucose tolerance test, insulin tolerance test and insulin release 
      test suggest that the impaired insulin secretion was significantly improved in 
      TLR4-/- HF mice, compared with the WT HF group. In TLR4-/- HF mice, islet beta cell 
      ultrastructure was not damaged in the face of the same high-fat continuous 
      stimulation, compared to that in the WT HF group. By detecting glucose-stimulated 
      insulin secretion in the primary islet, insulin secretion of TLR4-/- HF mice was 
      better than that of the WT HF group, and in the TLR4-/- HF group, at the mRNA 
      level, islet interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and monocyte 
      chemotactic protein 1 (MCP-1) were significantly lower than in the WT HF group. 
      There was the islet macrophage infiltration in the WT HF group, but no 
      significant macrophage infiltration in the TLR4-/- HF group. These data suggest 
      that the damaged islet functions of the high fat diet-induced obesity mice may be 
      linked to the TLR4 expression level, and the recruitment of macrophages into the 
      islets.
FAU - Li, Juan
AU  - Li J
AD  - Department of Clinical Nutrition, Changhai Hospital, Second Military Medical 
      University, Shanghai, PR China.
FAU - Chen, Shufen
AU  - Chen S
AD  - Department of Clinical Nutrition, Changhai Hospital, Second Military Medical 
      University, Shanghai, PR China.
FAU - Qiang, Juan
AU  - Qiang J
AD  - Department of Clinical Nutrition, Changhai Hospital, Second Military Medical 
      University, Shanghai, PR China.
FAU - Wang, Xin
AU  - Wang X
AD  - Department of Clinical Nutrition, Changhai Hospital, Second Military Medical 
      University, Shanghai, PR China.
FAU - Chen, Lei
AU  - Chen L
AD  - International Cooperation Laboratory on Signal Transduction, Eastern 
      Hepatobiliary Surgery Institute, Second Military Medical University, Shanghai, PR 
      China.
FAU - Zou, Dajin
AU  - Zou D
AD  - Department of Endocrinology, Changhai Hospital, Second Military Medical 
      University, Shanghai, PR China.
LA  - eng
PT  - Journal Article
DEP - 20141014
PL  - Poland
TA  - Cent Eur J Immunol
JT  - Central-European journal of immunology
JID - 9702239
PMC - PMC4439999
OTO - NOTNLM
OT  - TLR4
OT  - cytokine
OT  - insulin resistance
OT  - islet function
OT  - obesity
EDAT- 2014/01/01 00:00
MHDA- 2014/01/01 00:01
PMCR- 2014/01/01
CRDT- 2015/07/09 06:00
PHST- 2014/04/18 00:00 [received]
PHST- 2014/06/09 00:00 [accepted]
PHST- 2015/07/09 06:00 [entrez]
PHST- 2014/01/01 00:00 [pubmed]
PHST- 2014/01/01 00:01 [medline]
PHST- 2014/01/01 00:00 [pmc-release]
AID - 45940 [pii]
AID - 10.5114/ceji.2014.45940 [doi]
PST - ppublish
SO  - Cent Eur J Immunol. 2014;39(3):306-15. doi: 10.5114/ceji.2014.45940. Epub 2014 
      Oct 14.