PMID- 21607879
OWN - NLM
STAT- MEDLINE
DCOM- 20110920
LR  - 20211020
IS  - 1573-6881 (Electronic)
IS  - 0145-479X (Linking)
VI  - 43
IP  - 2
DP  - 2011 Apr
TI  - UCP4 overexpression improves fatty acid oxidation and insulin sensitivity in L6 
      myocytes.
PG  - 109-18
LID - 10.1007/s10863-011-9344-9 [doi]
AB  - Obesity, which is caused by energy uptake being greater than energy expenditure, 
      is widely prevalent today. Currently, only a limited number of efficient 
      interventional strategies are available for the prevention of obesity. Previous 
      studies have shown that UCP4 transcription occurs at a considerable level in 
      mouse skeletal muscle; however, the exact functions of UCP4 remain unclear. In 
      this study, we investigated the effect of UCP4 on mitochondrial function and 
      insulin sensitivity in mature L6 myocytes. UCP4 overexpression in L6 myocytes 
      induced increased mitochondrial carnitine palmitoyltransferase 1A (CPT1A) and 
      decreased citrate synthase (CS) mRNA in the basal condition (i.e., in the absence 
      of insulin). UCP4 overexpression significantly improved insulin sensitivity, 
      increased tyrosine phosphorylation of IRS-1 in the presence of insulin, and 
      significantly reduced intracellular triglyceride (TG). Additionally, 
      intracellular ATP content and mitochondrial membrane potential were 
      downregulated. We also observed that intracellular ROS, mitochondrial morphology, 
      and mitochondrial mtDNA copy number were maintained upon UCP4 expression, with no 
      change in mitochondrial fusion and fission. In summary, our findings provide 
      evidence to show that UCP4 overexpression reduced the insulin sensitivity and 
      mitochondrial fatty acid oxidation of L6 myocytes. These findings support the 
      notion that UCPs are ideal targets for treatment of insulin resistance.
FAU - Gao, Chun-Lin
AU  - Gao CL
AD  - Department of Pediatrics, Jinling Hospital, Nanjing, China.
FAU - Ni, Yu-Hui
AU  - Ni YH
FAU - Liu, Guanglin
AU  - Liu G
FAU - Chen, Xiao-Hui
AU  - Chen XH
FAU - Ji, Chen-Bo
AU  - Ji CB
FAU - Qin, Da-Ni
AU  - Qin DN
FAU - Kou, Chun-Zhao
AU  - Kou CZ
FAU - Zhu, Chun
AU  - Zhu C
FAU - Zhang, Chun-Mei
AU  - Zhang CM
FAU - Xia, Zheng-Kun
AU  - Xia ZK
FAU - Guo, Xi-Rong
AU  - Guo XR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110524
PL  - United States
TA  - J Bioenerg Biomembr
JT  - Journal of bioenergetics and biomembranes
JID - 7701859
RN  - 0 (Fatty Acids)
RN  - 0 (Insulin)
RN  - 0 (Ion Channels)
RN  - 0 (Mitochondrial Proteins)
RN  - 0 (Mitochondrial Uncoupling Proteins)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Slc25a27 protein, rat)
RN  - 0 (Triglycerides)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - Fatty Acids/genetics/*metabolism
MH  - Insulin/metabolism
MH  - *Insulin Resistance
MH  - Ion Channels/*biosynthesis/genetics
MH  - *Membrane Potential, Mitochondrial
MH  - Mice
MH  - Mitochondria, Muscle/*metabolism
MH  - Mitochondrial Proteins/*biosynthesis/genetics
MH  - Mitochondrial Uncoupling Proteins
MH  - Muscle Fibers, Skeletal/*metabolism
MH  - Obesity/genetics/metabolism
MH  - Oxidation-Reduction
MH  - Rats
MH  - Reactive Oxygen Species/metabolism
MH  - Triglycerides/genetics/metabolism
EDAT- 2011/05/25 06:00
MHDA- 2011/09/21 06:00
CRDT- 2011/05/25 06:00
PHST- 2010/06/06 00:00 [received]
PHST- 2010/11/12 00:00 [accepted]
PHST- 2011/05/25 06:00 [entrez]
PHST- 2011/05/25 06:00 [pubmed]
PHST- 2011/09/21 06:00 [medline]
AID - 10.1007/s10863-011-9344-9 [doi]
PST - ppublish
SO  - J Bioenerg Biomembr. 2011 Apr;43(2):109-18. doi: 10.1007/s10863-011-9344-9. Epub 
      2011 May 24.