Glucose transport activity in L6 muscle cells is regulated by the coordinate control of subcellular glucose transporter distribution, biosynthesis, and mRNA transcription

Patricia S. Walker, Toolsie Ramlal, Vivian Sarabia, Ulla Maija Koivisto, Philip J. Bilan, Jeffrey E. Pessin, Amira Klip

Research output: Contribution to journalArticle

84 Citations (Scopus)

Abstract

Chronic (24 h) insulin treatment and/or glucose deprivation of differentiated rat L6 skeletal muscle cells resulted in an increase in glucose transport activity and a 2-3-fold increase in the number of plasma membrane-associated cytochalasin B binding sites and immunoreactive glucose transporters. In contrast to the acute effect of insulin, chronic treatment did not decrease the number of cytochalasin B binding sites or immunoreactive glucose transporter proteins present in intracellular low density microsomes. Although acute insulin stimulation of glucose transport activity was not affected by cycloheximide, chronic insulin stimulation of glucose transport activity and glucose transporter protein were decreased. In contrast, the stimulation of glucose transport activity by both acute and chronic glucose deprivation were cycloheximide-insensitive. Previously we have reported that chronic insulin treatment transiently induces the rat brain/HepG2 glucose transporter subtype (GLUT-1) mRNA, whereas glucose deprivation induces a substained increase (Walker, P. S., Ramlal, T., Donovan, J. A., Doering, T. P., Sandra, A., Klip, A Pessin, J. E. (1989) J. Biol. Chem. 264, 6587-6595). Consistent with these data, nuclear run-on analysis demonstrated a transient 3-fold increase in the rate of GLUT-1 glucose transporter mRNA transcription induced by either chronic insulin treatment or glucose deprivation. The combination of chronic insulin treatment with glucose deprivation resulted in a more persistent 3-4-fold increase in transcription rate than either treatment alone. These data demonstrate that prolonged insulin- and glucose-dependent regulation of glucose transporter function occurs by a complex mechanism which includes enhanced GLUT-1 mRNA transcription and glucose transporter synthesis, as well as changes in the subcellular distribution of glucose transporter proteins.

Original languageEnglish (US)
Pages (from-to)1516-1523
Number of pages8
JournalJournal of Biological Chemistry
Volume265
Issue number3
StatePublished - Jan 25 1990
Externally publishedYes

Fingerprint

Facilitative Glucose Transport Proteins
Biosynthesis
Transcription
Muscle Cells
Muscle
Cells
Glucose
Messenger RNA
Insulin
Cytochalasin B
Cycloheximide
Rats
Binding Sites
Proteins
Cell membranes
Microsomes
Brain
Skeletal Muscle
Cell Membrane

ASJC Scopus subject areas

  • Biochemistry

Cite this

Glucose transport activity in L6 muscle cells is regulated by the coordinate control of subcellular glucose transporter distribution, biosynthesis, and mRNA transcription. / Walker, Patricia S.; Ramlal, Toolsie; Sarabia, Vivian; Koivisto, Ulla Maija; Bilan, Philip J.; Pessin, Jeffrey E.; Klip, Amira.

In: Journal of Biological Chemistry, Vol. 265, No. 3, 25.01.1990, p. 1516-1523.

Research output: Contribution to journalArticle

Walker, Patricia S. ; Ramlal, Toolsie ; Sarabia, Vivian ; Koivisto, Ulla Maija ; Bilan, Philip J. ; Pessin, Jeffrey E. ; Klip, Amira. / Glucose transport activity in L6 muscle cells is regulated by the coordinate control of subcellular glucose transporter distribution, biosynthesis, and mRNA transcription. In: Journal of Biological Chemistry. 1990 ; Vol. 265, No. 3. pp. 1516-1523.
@article{e68d7e11bf8e4f959e376dc0d4c1a3c3,
title = "Glucose transport activity in L6 muscle cells is regulated by the coordinate control of subcellular glucose transporter distribution, biosynthesis, and mRNA transcription",
abstract = "Chronic (24 h) insulin treatment and/or glucose deprivation of differentiated rat L6 skeletal muscle cells resulted in an increase in glucose transport activity and a 2-3-fold increase in the number of plasma membrane-associated cytochalasin B binding sites and immunoreactive glucose transporters. In contrast to the acute effect of insulin, chronic treatment did not decrease the number of cytochalasin B binding sites or immunoreactive glucose transporter proteins present in intracellular low density microsomes. Although acute insulin stimulation of glucose transport activity was not affected by cycloheximide, chronic insulin stimulation of glucose transport activity and glucose transporter protein were decreased. In contrast, the stimulation of glucose transport activity by both acute and chronic glucose deprivation were cycloheximide-insensitive. Previously we have reported that chronic insulin treatment transiently induces the rat brain/HepG2 glucose transporter subtype (GLUT-1) mRNA, whereas glucose deprivation induces a substained increase (Walker, P. S., Ramlal, T., Donovan, J. A., Doering, T. P., Sandra, A., Klip, A Pessin, J. E. (1989) J. Biol. Chem. 264, 6587-6595). Consistent with these data, nuclear run-on analysis demonstrated a transient 3-fold increase in the rate of GLUT-1 glucose transporter mRNA transcription induced by either chronic insulin treatment or glucose deprivation. The combination of chronic insulin treatment with glucose deprivation resulted in a more persistent 3-4-fold increase in transcription rate than either treatment alone. These data demonstrate that prolonged insulin- and glucose-dependent regulation of glucose transporter function occurs by a complex mechanism which includes enhanced GLUT-1 mRNA transcription and glucose transporter synthesis, as well as changes in the subcellular distribution of glucose transporter proteins.",
author = "Walker, {Patricia S.} and Toolsie Ramlal and Vivian Sarabia and Koivisto, {Ulla Maija} and Bilan, {Philip J.} and Pessin, {Jeffrey E.} and Amira Klip",
year = "1990",
month = "1",
day = "25",
language = "English (US)",
volume = "265",
pages = "1516--1523",
journal = "Journal of Biological Chemistry",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "3",

}

TY - JOUR

T1 - Glucose transport activity in L6 muscle cells is regulated by the coordinate control of subcellular glucose transporter distribution, biosynthesis, and mRNA transcription

AU - Walker, Patricia S.

AU - Ramlal, Toolsie

AU - Sarabia, Vivian

AU - Koivisto, Ulla Maija

AU - Bilan, Philip J.

AU - Pessin, Jeffrey E.

AU - Klip, Amira

PY - 1990/1/25

Y1 - 1990/1/25

N2 - Chronic (24 h) insulin treatment and/or glucose deprivation of differentiated rat L6 skeletal muscle cells resulted in an increase in glucose transport activity and a 2-3-fold increase in the number of plasma membrane-associated cytochalasin B binding sites and immunoreactive glucose transporters. In contrast to the acute effect of insulin, chronic treatment did not decrease the number of cytochalasin B binding sites or immunoreactive glucose transporter proteins present in intracellular low density microsomes. Although acute insulin stimulation of glucose transport activity was not affected by cycloheximide, chronic insulin stimulation of glucose transport activity and glucose transporter protein were decreased. In contrast, the stimulation of glucose transport activity by both acute and chronic glucose deprivation were cycloheximide-insensitive. Previously we have reported that chronic insulin treatment transiently induces the rat brain/HepG2 glucose transporter subtype (GLUT-1) mRNA, whereas glucose deprivation induces a substained increase (Walker, P. S., Ramlal, T., Donovan, J. A., Doering, T. P., Sandra, A., Klip, A Pessin, J. E. (1989) J. Biol. Chem. 264, 6587-6595). Consistent with these data, nuclear run-on analysis demonstrated a transient 3-fold increase in the rate of GLUT-1 glucose transporter mRNA transcription induced by either chronic insulin treatment or glucose deprivation. The combination of chronic insulin treatment with glucose deprivation resulted in a more persistent 3-4-fold increase in transcription rate than either treatment alone. These data demonstrate that prolonged insulin- and glucose-dependent regulation of glucose transporter function occurs by a complex mechanism which includes enhanced GLUT-1 mRNA transcription and glucose transporter synthesis, as well as changes in the subcellular distribution of glucose transporter proteins.

AB - Chronic (24 h) insulin treatment and/or glucose deprivation of differentiated rat L6 skeletal muscle cells resulted in an increase in glucose transport activity and a 2-3-fold increase in the number of plasma membrane-associated cytochalasin B binding sites and immunoreactive glucose transporters. In contrast to the acute effect of insulin, chronic treatment did not decrease the number of cytochalasin B binding sites or immunoreactive glucose transporter proteins present in intracellular low density microsomes. Although acute insulin stimulation of glucose transport activity was not affected by cycloheximide, chronic insulin stimulation of glucose transport activity and glucose transporter protein were decreased. In contrast, the stimulation of glucose transport activity by both acute and chronic glucose deprivation were cycloheximide-insensitive. Previously we have reported that chronic insulin treatment transiently induces the rat brain/HepG2 glucose transporter subtype (GLUT-1) mRNA, whereas glucose deprivation induces a substained increase (Walker, P. S., Ramlal, T., Donovan, J. A., Doering, T. P., Sandra, A., Klip, A Pessin, J. E. (1989) J. Biol. Chem. 264, 6587-6595). Consistent with these data, nuclear run-on analysis demonstrated a transient 3-fold increase in the rate of GLUT-1 glucose transporter mRNA transcription induced by either chronic insulin treatment or glucose deprivation. The combination of chronic insulin treatment with glucose deprivation resulted in a more persistent 3-4-fold increase in transcription rate than either treatment alone. These data demonstrate that prolonged insulin- and glucose-dependent regulation of glucose transporter function occurs by a complex mechanism which includes enhanced GLUT-1 mRNA transcription and glucose transporter synthesis, as well as changes in the subcellular distribution of glucose transporter proteins.

UR - http://www.scopus.com/inward/record.url?scp=0025058097&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025058097&partnerID=8YFLogxK

M3 - Article

VL - 265

SP - 1516

EP - 1523

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 3

ER -