PMID- 27872157
OWN - NLM
STAT- MEDLINE
DCOM- 20171207
LR  - 20181202
IS  - 1479-6813 (Electronic)
IS  - 0952-5041 (Linking)
VI  - 58
IP  - 2
DP  - 2017 Feb
TI  - Exendin-4 increases oxygen consumption and thermogenic gene expression in muscle 
      cells.
PG  - 79-90
LID - 10.1530/JME-16-0078 [doi]
AB  - Glucagon-like peptide-1 (GLP1) has many anti-diabetic actions and also increases 
      energy expenditure in vivo As skeletal muscle is a major organ controlling energy 
      metabolism, we investigated whether GLP1 can affect energy metabolism in muscle. 
      We found that treatment of differentiated C2C12 cells with exendin-4 (Ex-4), a 
      GLP1 receptor agonist, reduced oleate:palmitate-induced lipid accumulation and 
      triglyceride content compared with cells without Ex-4 treatment. When we examined 
      the oxygen consumption rate (OCR), not only the basal OCR but also the OCR 
      induced by oleate:palmitate addition was significantly increased in Ex-4-treated 
      differentiated C2C12 cells, and this was inhibited by exendin-9, a GLP1 receptor 
      antagonist. The expression of uncoupling protein 1 (UCP1), beta(3)-adrenergic 
      receptor, peroxisome proliferator-activator receptor a (PPARa) and farnesoid X 
      receptor mRNA was significantly upregulated in Ex-4-treated differentiated C2C12 
      cells, and the upregulation of these mRNA was abolished by treatment with 
      adenylate cyclase inhibitor (2'5'-dideoxyadenosine) or PKA inhibitor (H-89). As 
      well, intramuscular injection of Ex-4 into diet-induced obese mice significantly 
      increased the expression of UCP1, PPARa and p-AMPK in muscle. We suggest that 
      exposure to GLP1 increases energy expenditure in muscle through the upregulation 
      of fat oxidation and thermogenic gene expression, which may contribute to 
      reducing obesity and insulin resistance.
CI  - (c) 2017 Society for Endocrinology.
FAU - Choung, Jin-Seung
AU  - Choung JS
AD  - College of Pharmacy and Gachon Institute of Pharmaceutical ScienceGachon 
      University, Incheon, Republic of Korea.
AD  - Lee Gil Ya Cancer and Diabetes InstituteGachon University, Incheon, Republic of 
      Korea.
FAU - Lee, Young-Sun
AU  - Lee YS
AD  - Lee Gil Ya Cancer and Diabetes InstituteGachon University, Incheon, Republic of 
      Korea.
FAU - Jun, Hee-Sook
AU  - Jun HS
AD  - College of Pharmacy and Gachon Institute of Pharmaceutical ScienceGachon 
      University, Incheon, Republic of Korea hsjun@gachon.ac.kr.
AD  - Lee Gil Ya Cancer and Diabetes InstituteGachon University, Incheon, Republic of 
      Korea.
AD  - Gachon Medical Research InstituteGil Hospital, Incheon, Republic of Korea.
LA  - eng
PT  - Journal Article
DEP - 20161121
PL  - England
TA  - J Mol Endocrinol
JT  - Journal of molecular endocrinology
JID - 8902617
RN  - 0 (Fatty Acids)
RN  - 0 (Glucagon-Like Peptide-1 Receptor)
RN  - 0 (PPAR alpha)
RN  - 0 (Peptides)
RN  - 0 (Uncoupling Protein 1)
RN  - 0 (Venoms)
RN  - 89750-14-1 (Glucagon-Like Peptide 1)
RN  - 9P1872D4OL (Exenatide)
RN  - E0399OZS9N (Cyclic AMP)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - EC 3.1.1.13 (Sterol Esterase)
SB  - IM
MH  - Animals
MH  - Cyclic AMP/metabolism
MH  - Cyclic AMP-Dependent Protein Kinases
MH  - Energy Metabolism/drug effects/genetics
MH  - Exenatide
MH  - Fatty Acids/metabolism
MH  - Gene Expression Regulation/*drug effects
MH  - Glucagon-Like Peptide 1/metabolism
MH  - Glucagon-Like Peptide-1 Receptor/metabolism
MH  - Lipid Metabolism/drug effects
MH  - Male
MH  - Mice
MH  - Muscle Cells/*drug effects/*metabolism
MH  - Muscle, Skeletal/metabolism
MH  - Oxygen Consumption/*drug effects
MH  - PPAR alpha/metabolism
MH  - Peptides/*pharmacology
MH  - Sterol Esterase/genetics/metabolism
MH  - Thermogenesis/*drug effects/*genetics
MH  - Uncoupling Protein 1/metabolism
MH  - Venoms/*pharmacology
OTO - NOTNLM
OT  - UCP1
OT  - energy expenditure
OT  - fat oxidation
OT  - glucagon-like peptide-1 receptor agonist
OT  - muscle
EDAT- 2016/11/23 06:00
MHDA- 2017/12/08 06:00
CRDT- 2016/11/23 06:00
PHST- 2016/11/16 00:00 [received]
PHST- 2016/11/21 00:00 [accepted]
PHST- 2016/11/23 06:00 [pubmed]
PHST- 2017/12/08 06:00 [medline]
PHST- 2016/11/23 06:00 [entrez]
AID - JME-16-0078 [pii]
AID - 10.1530/JME-16-0078 [doi]
PST - ppublish
SO  - J Mol Endocrinol. 2017 Feb;58(2):79-90. doi: 10.1530/JME-16-0078. Epub 2016 Nov 
      21.