PMID- 24702712
OWN - NLM
STAT- MEDLINE
DCOM- 20150514
LR  - 20220129
IS  - 1463-1326 (Electronic)
IS  - 1462-8902 (Linking)
VI  - 16
IP  - 10
DP  - 2014 Oct
TI  - Interleukin-6 in combination with the interleukin-6 receptor stimulates glucose 
      uptake in resting human skeletal muscle independently of insulin action.
PG  - 931-6
LID - 10.1111/dom.12299 [doi]
AB  - AIM: To examine if the physiological concentrations of both interleukin-6 (IL-6), 
      in combination with IL-6 receptor (IL-6R), are able to stimulate glucose uptake 
      in human skeletal muscle and to identify the associated signalling pathways. 
      METHODS: Skeletal muscle tissue (~60 mg) obtained from healthy female volunteers 
      via muscle biopsy was subjected to incubation in the absence or presence of 
      insulin (60 microU/ml), recombinant human IL-6 (rhIL-6) (4 ng/ml) or a combination of 
      rhIL-6 (4 ng/ml) and rhIL-6R (100 ng/ml) for 30 min, with glucose transport 
      measured for each incubation. Western blot analysis was conducted on key 
      signalling proteins, protein kinase B (PKB/Akt), adenosine monophosphate kinase 
      (AMPK) and mammalian target of rapamycin (mTOR) to gain an early insight into any 
      differing transport mechanisms. RESULTS: Human skeletal muscle exhibited 
      increased glucose uptake with insulin (1.85-fold; p < 0.05) and stimulated 
      phosphorylation of PKB/Akt and AMPK (0.98 +/- 0.23 and 1.49 +/- 0.13, respectively, 
      phosphorylated: total; p < 0.05). IL-6/IL-6R increased phosphorylation of mTOR 
      (fourfold, p < 0.05) compared to insulin, IL-6 alone and basal control. IL-6 did 
      not stimulate glucose uptake but combined with IL-6R, induced 1.5-fold increase 
      in glucose uptake (p < 0.05) and phosphorylation of AMPK (0.95 +/- 0.19; 
      phosphorylated: total, p < 0.05). CONCLUSIONS: IL-6 in combination with IL-6R and 
      not IL-6 alone increased glucose uptake in human skeletal muscle. 
      IL-6/IL-6R-mediated glucose uptake occurred independently of PKB/Akt 
      phosphorylation, showing that IL-6/IL-6R-induced glucose uptake is dependent on a 
      divergent pathway.
CI  - (c) 2014 John Wiley & Sons Ltd.
FAU - Saini, A
AU  - Saini A
AD  - School of Sport, Exercise & Health Sciences, Loughborough University, 
      Loughborough, UK.
FAU - Faulkner, S H
AU  - Faulkner SH
FAU - Moir, H
AU  - Moir H
FAU - Warwick, P
AU  - Warwick P
FAU - King, J A
AU  - King JA
FAU - Nimmo, M A
AU  - Nimmo MA
LA  - eng
GR  - MR/K00414X/1/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140427
PL  - England
TA  - Diabetes Obes Metab
JT  - Diabetes, obesity & metabolism
JID - 100883645
RN  - 0 (Interleukin-6)
RN  - 0 (Receptors, Interleukin-6)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Biological Transport
MH  - Female
MH  - Glucose/*metabolism
MH  - Humans
MH  - Interleukin-6/*metabolism/pharmacology
MH  - Muscle, Skeletal/*metabolism/physiology
MH  - Phosphorylation
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Receptors, Interleukin-6/drug effects/*metabolism
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/*metabolism
OTO - NOTNLM
OT  - glucose uptake
OT  - human skeletal muscle
OT  - insulin
OT  - interleukin
OT  - interleukin-6 and receptor
EDAT- 2014/04/08 06:00
MHDA- 2015/05/15 06:00
CRDT- 2014/04/08 06:00
PHST- 2013/11/06 00:00 [received]
PHST- 2014/02/26 00:00 [revised]
PHST- 2014/03/31 00:00 [accepted]
PHST- 2014/04/08 06:00 [entrez]
PHST- 2014/04/08 06:00 [pubmed]
PHST- 2015/05/15 06:00 [medline]
AID - 10.1111/dom.12299 [doi]
PST - ppublish
SO  - Diabetes Obes Metab. 2014 Oct;16(10):931-6. doi: 10.1111/dom.12299. Epub 2014 Apr 
      27.