PMID- 33613155
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220420
IS  - 1654-661X (Print)
IS  - 1654-661X (Electronic)
IS  - 1654-661X (Linking)
VI  - 65
DP  - 2021
TI  - Pentadecanoic acid promotes basal and insulin-stimulated glucose uptake in C2C12 
      myotubes.
LID - 10.29219/fnr.v65.4527 [doi]
AB  - BACKGROUND: Saturated fatty acids (SFAs) generally have been thought to worsen 
      insulin-resistance and increase the risk of developing type 2 diabetes mellitus 
      (T2DM). Recently, accumulating evidence has revealed that SFAs are not a single 
      homogeneous group, instead different SFAs are associated with T2DM in opposing 
      directions. Pentadecanoic acid (C15:0, PA) is directly correlated with dairy 
      products, and a negative association between circulating PA and metabolic disease 
      risk was observed in epidemiological studies. Therefore, the role of PA in human 
      health needs to be reinforced. Whether PA has a direct benefit on glucose 
      metabolism and insulin sensitivity needs further investigation. OBJECTIVE: The 
      present study aimed to investigate the effect and potential mechanism of action 
      of PA on basal and insulin stimulated glucose uptake in C2C12 myotubes. METHODS: 
      Glucose uptake was determined using a 2-(N-[7-nitrobenz-2-oxa-1,3-diazol-4-yl] 
      amino)-2-deoxyglucose (2-NBDG) uptake assay. Cell membrane proteins were isolated 
      and glucose transporter 4 (GLUT4) protein was detected by western blotting to 
      examine the translocation of GLUT4 to the plasma membrane. The phosphorylation 
      levels of proteins involved in the insulin and 5'-adenosine 
      monophosphate-activated protein kinase (AMPK) pathways were examined by western 
      blotting. RESULTS: We found that PA significantly promoted glucose uptake and 
      GLUT4 translocation to the plasma membrane. PA had no effect on the 
      insulin-dependent pathway involving insulin receptor substrate 1 (Tyr632) and 
      protein kinase B (PKB/Akt), but increased phosphorylation of AMPK and Akt 
      substrate of 160 kDa (AS160). Compound C (an AMPK inhibitor) blocked PA-induced 
      AMPK activation and reversed PA-induced GLUT4 translocation, indicating that PA 
      promotes glucose uptake via the AMPK pathway in vitro. Moreover, PA significantly 
      promoted insulin-stimulated glucose uptake in myotubes. Under insulin 
      stimulation, PA did not affect the insulin-dependent pathway, but still activated 
      AMPK. CONCLUSION: PA, an odd-chain SFA, significantly stimulates glucose uptake 
      via the AMPK-AS160 pathway and exhibits an insulin-sensitizing effect in 
      myotubes.
CI  - (c) Fu et al.
FAU - Fu, Wen-Cheng
AU  - Fu WC
AD  - School of Life Sciences, East China Normal University, Shanghai, China.
FAU - Li, Hai-Yan
AU  - Li HY
AD  - School of Life Sciences, East China Normal University, Shanghai, China.
FAU - Li, Tian-Tian
AU  - Li TT
AD  - School of Life Sciences, East China Normal University, Shanghai, China.
FAU - Yang, Kuo
AU  - Yang K
AD  - School of Life Sciences, East China Normal University, Shanghai, China.
FAU - Chen, Jia-Xiang
AU  - Chen JX
AD  - School of Life Sciences, East China Normal University, Shanghai, China.
FAU - Wang, Si-Jia
AU  - Wang SJ
AD  - School of Life Sciences, East China Normal University, Shanghai, China.
FAU - Liu, Chun-Hui
AU  - Liu CH
AD  - China National Institute of Standardization, Beijing, China.
FAU - Zhang, Wen
AU  - Zhang W
AD  - School of Life Sciences, East China Normal University, Shanghai, China.
LA  - eng
PT  - Journal Article
DEP - 20210122
PL  - Sweden
TA  - Food Nutr Res
JT  - Food & nutrition research
JID - 101488795
PMC - PMC7869443
OTO - NOTNLM
OT  - AMP-activated protein kinase
OT  - C2C12 myotubes
OT  - glucose uptake
OT  - insulin sensitivity
OT  - pentadecanoic acid
COIS- All authors declare no conflicts of interest. This work was supported by Shanghai 
      Committee of Science and Technology Major Program (NO. 11DJ1400101) and grants 
      from the China national institute of standardization.
EDAT- 2021/02/23 06:00
MHDA- 2021/02/23 06:01
PMCR- 2021/01/22
CRDT- 2021/02/22 05:52
PHST- 2020/03/15 00:00 [received]
PHST- 2020/12/21 00:00 [revised]
PHST- 2020/12/21 00:00 [accepted]
PHST- 2021/02/22 05:52 [entrez]
PHST- 2021/02/23 06:00 [pubmed]
PHST- 2021/02/23 06:01 [medline]
PHST- 2021/01/22 00:00 [pmc-release]
AID - 4527 [pii]
AID - 10.29219/fnr.v65.4527 [doi]
PST - epublish
SO  - Food Nutr Res. 2021 Jan 22;65. doi: 10.29219/fnr.v65.4527. eCollection 2021.