Regulation of glucose transporter messenger RNA in insulin-deficient states

William I. Sivitz, Susan L. DeSautel, Toshiaki Kayano, Graeme I. Bell, Jeffrey E. Pessin

Research output: Contribution to journalArticle

204 Citations (Scopus)

Abstract

Recent studies have indicated that a family of structurally related proteins with distinct but overlapping tissue distributions are responsible for facilitative glucose transport in mammalian tissues1-13. Insulin primarily stimulates glucose transport by inducing the redistribution of a unique glucose transporter protein from an intracellular pool to the plasma membrane3. This 509-amino-acid integral membrane protein, termed GLUT-4 (ref. 2), is the main insulin-responsive glucose transporter in adipose and muscle tissues1-3. We have observed a dramatic decrease (tenfold) in the steady-state levels of GLUT-4 messenger RNA in adipose tissue from fasted rats or rats made insulin deficient with streptozotocin. Insulin treatment of the streptozotocin-diabetic rats or refeeding the fasted animals causes a rapid recovery of the GLUT-4 mRNA to levels significantly above those observed in untreated control animals. By contrast, the levels of the erythrocyte/HepG2/rat brain-type glucose transporter mRNA remain essentially unchanged under these conditions. These data suggest that the in vivo expression of GLUT-4 mRNA in rat adipose tissue is regulated by insulin.

Original languageEnglish (US)
Pages (from-to)72-74
Number of pages3
JournalNature
Volume340
Issue number6228
StatePublished - 1989
Externally publishedYes

Fingerprint

Facilitative Glucose Transport Proteins
Insulin
Messenger RNA
Streptozocin
Adipose Tissue
Glucose Transporter Type 4
Glucose
Tissue Distribution
Membrane Proteins
Proteins
Erythrocytes
Amino Acids
Muscles
Brain

ASJC Scopus subject areas

  • General

Cite this

Sivitz, W. I., DeSautel, S. L., Kayano, T., Bell, G. I., & Pessin, J. E. (1989). Regulation of glucose transporter messenger RNA in insulin-deficient states. Nature, 340(6228), 72-74.

Regulation of glucose transporter messenger RNA in insulin-deficient states. / Sivitz, William I.; DeSautel, Susan L.; Kayano, Toshiaki; Bell, Graeme I.; Pessin, Jeffrey E.

In: Nature, Vol. 340, No. 6228, 1989, p. 72-74.

Research output: Contribution to journalArticle

Sivitz, WI, DeSautel, SL, Kayano, T, Bell, GI & Pessin, JE 1989, 'Regulation of glucose transporter messenger RNA in insulin-deficient states', Nature, vol. 340, no. 6228, pp. 72-74.
Sivitz WI, DeSautel SL, Kayano T, Bell GI, Pessin JE. Regulation of glucose transporter messenger RNA in insulin-deficient states. Nature. 1989;340(6228):72-74.
Sivitz, William I. ; DeSautel, Susan L. ; Kayano, Toshiaki ; Bell, Graeme I. ; Pessin, Jeffrey E. / Regulation of glucose transporter messenger RNA in insulin-deficient states. In: Nature. 1989 ; Vol. 340, No. 6228. pp. 72-74.
@article{44ee168879ac420496f4c10effebac9f,
title = "Regulation of glucose transporter messenger RNA in insulin-deficient states",
abstract = "Recent studies have indicated that a family of structurally related proteins with distinct but overlapping tissue distributions are responsible for facilitative glucose transport in mammalian tissues1-13. Insulin primarily stimulates glucose transport by inducing the redistribution of a unique glucose transporter protein from an intracellular pool to the plasma membrane3. This 509-amino-acid integral membrane protein, termed GLUT-4 (ref. 2), is the main insulin-responsive glucose transporter in adipose and muscle tissues1-3. We have observed a dramatic decrease (tenfold) in the steady-state levels of GLUT-4 messenger RNA in adipose tissue from fasted rats or rats made insulin deficient with streptozotocin. Insulin treatment of the streptozotocin-diabetic rats or refeeding the fasted animals causes a rapid recovery of the GLUT-4 mRNA to levels significantly above those observed in untreated control animals. By contrast, the levels of the erythrocyte/HepG2/rat brain-type glucose transporter mRNA remain essentially unchanged under these conditions. These data suggest that the in vivo expression of GLUT-4 mRNA in rat adipose tissue is regulated by insulin.",
author = "Sivitz, {William I.} and DeSautel, {Susan L.} and Toshiaki Kayano and Bell, {Graeme I.} and Pessin, {Jeffrey E.}",
year = "1989",
language = "English (US)",
volume = "340",
pages = "72--74",
journal = "Nature",
issn = "0028-0836",
publisher = "Nature Publishing Group",
number = "6228",

}

TY - JOUR

T1 - Regulation of glucose transporter messenger RNA in insulin-deficient states

AU - Sivitz, William I.

AU - DeSautel, Susan L.

AU - Kayano, Toshiaki

AU - Bell, Graeme I.

AU - Pessin, Jeffrey E.

PY - 1989

Y1 - 1989

N2 - Recent studies have indicated that a family of structurally related proteins with distinct but overlapping tissue distributions are responsible for facilitative glucose transport in mammalian tissues1-13. Insulin primarily stimulates glucose transport by inducing the redistribution of a unique glucose transporter protein from an intracellular pool to the plasma membrane3. This 509-amino-acid integral membrane protein, termed GLUT-4 (ref. 2), is the main insulin-responsive glucose transporter in adipose and muscle tissues1-3. We have observed a dramatic decrease (tenfold) in the steady-state levels of GLUT-4 messenger RNA in adipose tissue from fasted rats or rats made insulin deficient with streptozotocin. Insulin treatment of the streptozotocin-diabetic rats or refeeding the fasted animals causes a rapid recovery of the GLUT-4 mRNA to levels significantly above those observed in untreated control animals. By contrast, the levels of the erythrocyte/HepG2/rat brain-type glucose transporter mRNA remain essentially unchanged under these conditions. These data suggest that the in vivo expression of GLUT-4 mRNA in rat adipose tissue is regulated by insulin.

AB - Recent studies have indicated that a family of structurally related proteins with distinct but overlapping tissue distributions are responsible for facilitative glucose transport in mammalian tissues1-13. Insulin primarily stimulates glucose transport by inducing the redistribution of a unique glucose transporter protein from an intracellular pool to the plasma membrane3. This 509-amino-acid integral membrane protein, termed GLUT-4 (ref. 2), is the main insulin-responsive glucose transporter in adipose and muscle tissues1-3. We have observed a dramatic decrease (tenfold) in the steady-state levels of GLUT-4 messenger RNA in adipose tissue from fasted rats or rats made insulin deficient with streptozotocin. Insulin treatment of the streptozotocin-diabetic rats or refeeding the fasted animals causes a rapid recovery of the GLUT-4 mRNA to levels significantly above those observed in untreated control animals. By contrast, the levels of the erythrocyte/HepG2/rat brain-type glucose transporter mRNA remain essentially unchanged under these conditions. These data suggest that the in vivo expression of GLUT-4 mRNA in rat adipose tissue is regulated by insulin.

UR - http://www.scopus.com/inward/record.url?scp=0024386710&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024386710&partnerID=8YFLogxK

M3 - Article

C2 - 2662016

AN - SCOPUS:0024386710

VL - 340

SP - 72

EP - 74

JO - Nature

JF - Nature

SN - 0028-0836

IS - 6228

ER -