Mechanisms limiting glycogen storage in muscle during prolonged insulin stimulation

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Mechanisms limiting glycogen storage in muscle during prolonged insulin stimulation. / Richter, Erik A.; Hansen, S A; Hansen, B F.

I: American Journal of Physiology (Consolidated), Bind 255, Nr. 5 Pt 1, 1988, s. E621-E628.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Richter, EA, Hansen, SA & Hansen, BF 1988, 'Mechanisms limiting glycogen storage in muscle during prolonged insulin stimulation', American Journal of Physiology (Consolidated), bind 255, nr. 5 Pt 1, s. E621-E628.

APA

Richter, E. A., Hansen, S. A., & Hansen, B. F. (1988). Mechanisms limiting glycogen storage in muscle during prolonged insulin stimulation. American Journal of Physiology (Consolidated), 255(5 Pt 1), E621-E628.

Vancouver

Richter EA, Hansen SA, Hansen BF. Mechanisms limiting glycogen storage in muscle during prolonged insulin stimulation. American Journal of Physiology (Consolidated). 1988;255(5 Pt 1):E621-E628.

Author

Richter, Erik A. ; Hansen, S A ; Hansen, B F. / Mechanisms limiting glycogen storage in muscle during prolonged insulin stimulation. I: American Journal of Physiology (Consolidated). 1988 ; Bind 255, Nr. 5 Pt 1. s. E621-E628.

Bibtex

@article{704d07263ec24a37b96e47e88f6906fe,
title = "Mechanisms limiting glycogen storage in muscle during prolonged insulin stimulation",
abstract = "The extent to which muscle glycogen concentrations can be increased during exposure to maximal insulin concentrations and abundant glucose was investigated in the isolated perfused rat hindquarter preparation. Perfusion for 7 h in the presence of 20,000 microU/ml insulin and 11-13 mM glucose increased muscle glycogen concentrations to maximal values 2, 3, and 3.5 times above normal fed levels in fast-twitch white, slow-twitch red, and fast-twitch red fibers, respectively. Glucose uptake decreased (mean +/- SE) from 34.9 +/- 1.2 mumol.g-1.h-1 at 0 h to 7.5 +/- 0.7 after 7 h of perfusion. During the perfusion muscle glycogen synthase activity decreased and free intracellular glucose and glucose 6-phosphate increased indicating that glucose disposal was impaired. However, glucose transport as measured by the uptake of 3-O-[14C]methyl-D-glucose was also markedly decreased after 5 and 7 h of perfusion compared with initial values. Total muscle water concentration decreased during glycogen loading of the muscles. Mechanisms limiting glycogen storage under maximal insulin stimulation include impaired insulin-stimulated membrane transport of glucose as well as impaired intracellular glucose disposal.",
keywords = "Adenosine Triphosphate, Animals, Glucose, Glucosephosphates, Glycogen, Glycogen Synthase, In Vitro Techniques, Insulin, Male, Muscles, Oxygen Consumption, Phosphocreatine, Rats, Rats, Inbred Strains, Stimulation, Chemical, Time Factors, Water",
author = "Richter, {Erik A.} and Hansen, {S A} and Hansen, {B F}",
year = "1988",
language = "English",
volume = "255",
pages = "E621--E628",
journal = "American Journal of Physiology - Cell Physiology",
issn = "0363-6143",
publisher = "American Physiological Society",
number = "5 Pt 1",

}

RIS

TY - JOUR

T1 - Mechanisms limiting glycogen storage in muscle during prolonged insulin stimulation

AU - Richter, Erik A.

AU - Hansen, S A

AU - Hansen, B F

PY - 1988

Y1 - 1988

N2 - The extent to which muscle glycogen concentrations can be increased during exposure to maximal insulin concentrations and abundant glucose was investigated in the isolated perfused rat hindquarter preparation. Perfusion for 7 h in the presence of 20,000 microU/ml insulin and 11-13 mM glucose increased muscle glycogen concentrations to maximal values 2, 3, and 3.5 times above normal fed levels in fast-twitch white, slow-twitch red, and fast-twitch red fibers, respectively. Glucose uptake decreased (mean +/- SE) from 34.9 +/- 1.2 mumol.g-1.h-1 at 0 h to 7.5 +/- 0.7 after 7 h of perfusion. During the perfusion muscle glycogen synthase activity decreased and free intracellular glucose and glucose 6-phosphate increased indicating that glucose disposal was impaired. However, glucose transport as measured by the uptake of 3-O-[14C]methyl-D-glucose was also markedly decreased after 5 and 7 h of perfusion compared with initial values. Total muscle water concentration decreased during glycogen loading of the muscles. Mechanisms limiting glycogen storage under maximal insulin stimulation include impaired insulin-stimulated membrane transport of glucose as well as impaired intracellular glucose disposal.

AB - The extent to which muscle glycogen concentrations can be increased during exposure to maximal insulin concentrations and abundant glucose was investigated in the isolated perfused rat hindquarter preparation. Perfusion for 7 h in the presence of 20,000 microU/ml insulin and 11-13 mM glucose increased muscle glycogen concentrations to maximal values 2, 3, and 3.5 times above normal fed levels in fast-twitch white, slow-twitch red, and fast-twitch red fibers, respectively. Glucose uptake decreased (mean +/- SE) from 34.9 +/- 1.2 mumol.g-1.h-1 at 0 h to 7.5 +/- 0.7 after 7 h of perfusion. During the perfusion muscle glycogen synthase activity decreased and free intracellular glucose and glucose 6-phosphate increased indicating that glucose disposal was impaired. However, glucose transport as measured by the uptake of 3-O-[14C]methyl-D-glucose was also markedly decreased after 5 and 7 h of perfusion compared with initial values. Total muscle water concentration decreased during glycogen loading of the muscles. Mechanisms limiting glycogen storage under maximal insulin stimulation include impaired insulin-stimulated membrane transport of glucose as well as impaired intracellular glucose disposal.

KW - Adenosine Triphosphate

KW - Animals

KW - Glucose

KW - Glucosephosphates

KW - Glycogen

KW - Glycogen Synthase

KW - In Vitro Techniques

KW - Insulin

KW - Male

KW - Muscles

KW - Oxygen Consumption

KW - Phosphocreatine

KW - Rats

KW - Rats, Inbred Strains

KW - Stimulation, Chemical

KW - Time Factors

KW - Water

M3 - Journal article

C2 - 3142271

VL - 255

SP - E621-E628

JO - American Journal of Physiology - Cell Physiology

JF - American Journal of Physiology - Cell Physiology

SN - 0363-6143

IS - 5 Pt 1

ER -

ID: 154757367