PMID- 21177945
OWN - NLM
STAT- MEDLINE
DCOM- 20110411
LR  - 20211020
IS  - 1477-9145 (Electronic)
IS  - 0022-0949 (Print)
IS  - 0022-0949 (Linking)
VI  - 214
IP  - Pt 2
DP  - 2011 Jan 15
TI  - The physiological regulation of glucose flux into muscle in vivo.
PG  - 254-62
LID - 10.1242/jeb.048041 [doi]
AB  - Skeletal muscle glucose uptake increases dramatically in response to physical 
      exercise. Moreover, skeletal muscle comprises the vast majority of 
      insulin-sensitive tissue and is a site of dysregulation in the insulin-resistant 
      state. The biochemical and histological composition of the muscle is well defined 
      in a variety of species. However, the functional consequences of muscle 
      biochemical and histological adaptations to physiological and pathophysiological 
      conditions are not well understood. The physiological regulation of muscle 
      glucose uptake is complex. Sites involved in the regulation of muscle glucose 
      uptake are defined by a three-step process consisting of: (1) delivery of glucose 
      to muscle, (2) transport of glucose into the muscle by GLUT4 and (3) 
      phosphorylation of glucose within the muscle by a hexokinase (HK). Muscle blood 
      flow, capillary recruitment and extracellular matrix characteristics determine 
      glucose movement from the blood to the interstitium. Plasma membrane GLUT4 
      content determines glucose transport into the cell. Muscle HK activity, cellular 
      HK compartmentalization and the concentration of the HK inhibitor glucose 
      6-phosphate determine the capacity to phosphorylate glucose. Phosphorylation of 
      glucose is irreversible in muscle; therefore, with this reaction, glucose is 
      trapped and the uptake process is complete. Emphasis has been placed on the role 
      of the glucose transport step for glucose influx into muscle with the past 
      assertion that membrane transport is rate limiting. More recent research 
      definitively shows that the distributed control paradigm more accurately defines 
      the regulation of muscle glucose uptake as each of the three steps that define 
      this process are important sites of flux control.
FAU - Wasserman, David H
AU  - Wasserman DH
AD  - Department of Molecular Physiology and Biophysics and the Mouse Metabolic 
      Phenotyping Center, Vanderbilt University School of Medicine, Nashville, TN 
      37232, USA. david.wasserman@vanderbilt.edu
FAU - Kang, Li
AU  - Kang L
FAU - Ayala, Julio E
AU  - Ayala JE
FAU - Fueger, Patrick T
AU  - Fueger PT
FAU - Lee-Young, Robert S
AU  - Lee-Young RS
LA  - eng
GR  - R37 DK050277/DK/NIDDK NIH HHS/United States
GR  - DK54902/DK/NIDDK NIH HHS/United States
GR  - DK50277/DK/NIDDK NIH HHS/United States
GR  - DK59637/DK/NIDDK NIH HHS/United States
GR  - R01 DK054902/DK/NIDDK NIH HHS/United States
GR  - U24 DK059637/DK/NIDDK NIH HHS/United States
GR  - R01 DK050277/DK/NIDDK NIH HHS/United States
GR  - R56 DK054902/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - England
TA  - J Exp Biol
JT  - The Journal of experimental biology
JID - 0243705
RN  - 0 (Glucose Transporter Type 4)
RN  - 0 (Insulin)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - AMP-Activated Protein Kinases/metabolism
MH  - Animals
MH  - Biological Transport
MH  - Exercise
MH  - Glucose/*metabolism
MH  - Glucose Transporter Type 4/metabolism
MH  - Humans
MH  - Insulin/metabolism
MH  - Insulin Resistance
MH  - Muscle, Skeletal/*metabolism
MH  - Nitric Oxide Synthase/metabolism
MH  - Phosphorylation
PMC - PMC3008632
EDAT- 2010/12/24 06:00
MHDA- 2011/04/13 06:00
PMCR- 2012/01/15
CRDT- 2010/12/24 06:00
PHST- 2010/12/24 06:00 [entrez]
PHST- 2010/12/24 06:00 [pubmed]
PHST- 2011/04/13 06:00 [medline]
PHST- 2012/01/15 00:00 [pmc-release]
AID - 214/2/254 [pii]
AID - 10.1242/jeb.048041 [doi]
PST - ppublish
SO  - J Exp Biol. 2011 Jan 15;214(Pt 2):254-62. doi: 10.1242/jeb.048041.