PMID- 27984084
OWN - NLM
STAT- MEDLINE
DCOM- 20180223
LR  - 20211204
IS  - 1872-8057 (Electronic)
IS  - 0303-7207 (Linking)
VI  - 439
DP  - 2017 Jan 5
TI  - Eicosapentaenoic acid abolishes inhibition of insulin-induced mTOR 
      phosphorylation by LPS via PTP1B downregulation in skeletal muscle.
PG  - 116-125
LID - S0303-7207(16)30440-3 [pii]
LID - 10.1016/j.mce.2016.10.029 [doi]
AB  - Dietary n-3 polyunsaturated fatty acids (n-3 PUFAs) increase insulin signaling in 
      skeletal muscle. In the current study, we investigated the effect of 
      eicosapentaenoic acid (EPA) on insulin-induced mammalian target of rapamycin 
      (mTOR) phosphorylation in myotubes. We showed that EPA did not affect basal and 
      insulin-induced mTOR phosphorylation in myotubes. However, EPA abolished 
      lipopolysaccharide (LPS) -induced deficiency in insulin signaling (P < 0.05). 
      Pre-incubation of nuclear factor kappaB (NF-kappaBeta) and c-Jun N-terminal kinases (JNK) 
      inhibitors prevented the decreased insulin-induced mTOR phosphorylation elicited 
      by LPS (P < 0.05). In addition, in protein tyrosine phosphatase-1B (PTP1B) 
      knockdown myotubes, LPS failed to decrease insulin-induced mammalian target of 
      rapamycin (mTOR) phosphorylation in myotubes (P > 0.05). In myotubes, LPS 
      stimulated PTP1B expression via NF-kappaB and activation protein-1 (AP1). 
      Pre-incubation of 50 muM EPA prevented the LPS-induced activation of AP1 and NF-kappaBeta 
      as well as PTP1B expression (P < 0.05). Interestingly, incubation of peroxisome 
      proliferator-activated receptor gamma (PPARgamma) antagonist (GW9662) prior to EPA 
      treatment, the effect of EPA on insulin-induced mTOR phosphorylation was blocked. 
      Accordingly, EPA did not inhibit the LPS-induced activation of AP1 or NF-kappaBeta as 
      well as PTP1B expression when incubation of GW9662 prior to EPA treatment. The 
      in vivo study showed that EPA prevented LPS-induced PTPT1B expression and a 
      decrease in insulin-induced mTOR phosphorylation in muscle of mice. In summary, 
      EPA abolished LPS inhibition of insulin-induced mTOR phosphorylation in myotubes, 
      and one of the key mechanisms was to inhibit AP1 and NF-kappaB activation and PTP1B 
      transcription.
CI  - Copyright (c) 2016 Elsevier Ireland Ltd. All rights reserved.
FAU - Wei, Hong-Kui
AU  - Wei HK
AD  - Department of Animal Nutrition and Feed Science, College of Animal Science and 
      Technology, Huazhong Agricultural University, 430070, Wuhan, PR China.
FAU - Deng, Zhao
AU  - Deng Z
AD  - Department of Animal Nutrition and Feed Science, College of Animal Science and 
      Technology, Huazhong Agricultural University, 430070, Wuhan, PR China.
FAU - Jiang, Shu-Zhong
AU  - Jiang SZ
AD  - Department of Animal Nutrition and Feed Science, College of Animal Science and 
      Technology, Huazhong Agricultural University, 430070, Wuhan, PR China.
FAU - Song, Tong-Xing
AU  - Song TX
AD  - Department of Animal Nutrition and Feed Science, College of Animal Science and 
      Technology, Huazhong Agricultural University, 430070, Wuhan, PR China.
FAU - Zhou, Yuan-Fei
AU  - Zhou YF
AD  - Department of Animal Nutrition and Feed Science, College of Animal Science and 
      Technology, Huazhong Agricultural University, 430070, Wuhan, PR China.
FAU - Peng, Jian
AU  - Peng J
AD  - Department of Animal Nutrition and Feed Science, College of Animal Science and 
      Technology, Huazhong Agricultural University, 430070, Wuhan, PR China. Electronic 
      address: pengjian@mail.hzau.edu.cn.
FAU - Tao, Ya-Xiong
AU  - Tao YX
AD  - Department of Anatomy, Physiology and Pharmacology, College of Veterinary 
      Medicine, Auburn University, AL 36849, USA. Electronic address: 
      taoyaxi@auburn.edu.
LA  - eng
PT  - Journal Article
DEP - 20161028
PL  - Ireland
TA  - Mol Cell Endocrinol
JT  - Molecular and cellular endocrinology
JID - 7500844
RN  - 0 (Insulin)
RN  - 0 (Lipopolysaccharides)
RN  - AAN7QOV9EA (Eicosapentaenoic Acid)
RN  - EC 2.7.1.1 (mTOR protein, mouse)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 1)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Down-Regulation/drug effects
MH  - Eicosapentaenoic Acid/*pharmacology
MH  - Insulin/*pharmacology
MH  - Lipopolysaccharides/*pharmacology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Muscle Fibers, Skeletal/drug effects/metabolism
MH  - Muscle, Skeletal/*drug effects/metabolism
MH  - Phosphorylation/drug effects
MH  - Protein Tyrosine Phosphatase, Non-Receptor Type 1/drug effects/*metabolism
MH  - Signal Transduction/drug effects
MH  - TOR Serine-Threonine Kinases/*metabolism
OTO - NOTNLM
OT  - Eicosapentaenoic acid
OT  - Insulin
OT  - Lipopolysaccharide
OT  - Mammalian target of rapamycin
OT  - Myotubes
EDAT- 2016/12/17 06:00
MHDA- 2018/02/24 06:00
CRDT- 2016/12/17 06:00
PHST- 2015/11/27 00:00 [received]
PHST- 2016/10/01 00:00 [revised]
PHST- 2016/10/26 00:00 [accepted]
PHST- 2016/12/17 06:00 [pubmed]
PHST- 2018/02/24 06:00 [medline]
PHST- 2016/12/17 06:00 [entrez]
AID - S0303-7207(16)30440-3 [pii]
AID - 10.1016/j.mce.2016.10.029 [doi]
PST - ppublish
SO  - Mol Cell Endocrinol. 2017 Jan 5;439:116-125. doi: 10.1016/j.mce.2016.10.029. Epub 
      2016 Oct 28.