Preservation of glucose metabolism in hypertrophic GLUT4-null hearts

Antine E. Stenbit, Ellen B. Katz, John C. Chatham, David L. Geenen, Stephen M. Factor, Robert G. Weiss, Tsu Shuen Tsao, Ashwani Malhotra, V. P. Chacko, Christopher Ocampo, Linda A. Jelicks, Maureen J. Charron

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

GLUT4-null mice lacking the insulin-sensitive glucose transporter are not diabetic but do exhibit abnormalities in glucose and lipid metabolism. The most striking morphological consequence of ablating GLUT4 is cardiac hypertrophy. GLUT4-null hearts display characteristics of hypertrophy caused by hypertension. However, GLUT4-null mice have normal blood pressure and maintain a normal cardiac contractile protein profile. Unexpectedly, although they lack the predominant glucose transporter in the heart, GLUT4-null hearts transport glucose and synthesize glycogen at normal levels, but gene expression of rate-limiting enzymes involved in fatty acid oxidation is decreased. The GLUT4-null heart represents a unique model of hypertrophy that may be used to study the consequences of altered substrate utilization in normal and pathophysiological conditions.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume279
Issue number1 48-1
StatePublished - 2000

Fingerprint

Glucose
Facilitative Glucose Transport Proteins
Hypertrophy
Contractile Proteins
Cardiomegaly
Glycogen
Lipid Metabolism
Fatty Acids
Insulin
Blood Pressure
Hypertension
Gene Expression
Enzymes

Keywords

  • Glycogen
  • Nuclear magnetic resonance
  • Transport

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Stenbit, A. E., Katz, E. B., Chatham, J. C., Geenen, D. L., Factor, S. M., Weiss, R. G., ... Charron, M. J. (2000). Preservation of glucose metabolism in hypertrophic GLUT4-null hearts. American Journal of Physiology - Heart and Circulatory Physiology, 279(1 48-1).

Preservation of glucose metabolism in hypertrophic GLUT4-null hearts. / Stenbit, Antine E.; Katz, Ellen B.; Chatham, John C.; Geenen, David L.; Factor, Stephen M.; Weiss, Robert G.; Tsao, Tsu Shuen; Malhotra, Ashwani; Chacko, V. P.; Ocampo, Christopher; Jelicks, Linda A.; Charron, Maureen J.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 279, No. 1 48-1, 2000.

Research output: Contribution to journalArticle

Stenbit, AE, Katz, EB, Chatham, JC, Geenen, DL, Factor, SM, Weiss, RG, Tsao, TS, Malhotra, A, Chacko, VP, Ocampo, C, Jelicks, LA & Charron, MJ 2000, 'Preservation of glucose metabolism in hypertrophic GLUT4-null hearts', American Journal of Physiology - Heart and Circulatory Physiology, vol. 279, no. 1 48-1.
Stenbit AE, Katz EB, Chatham JC, Geenen DL, Factor SM, Weiss RG et al. Preservation of glucose metabolism in hypertrophic GLUT4-null hearts. American Journal of Physiology - Heart and Circulatory Physiology. 2000;279(1 48-1).
Stenbit, Antine E. ; Katz, Ellen B. ; Chatham, John C. ; Geenen, David L. ; Factor, Stephen M. ; Weiss, Robert G. ; Tsao, Tsu Shuen ; Malhotra, Ashwani ; Chacko, V. P. ; Ocampo, Christopher ; Jelicks, Linda A. ; Charron, Maureen J. / Preservation of glucose metabolism in hypertrophic GLUT4-null hearts. In: American Journal of Physiology - Heart and Circulatory Physiology. 2000 ; Vol. 279, No. 1 48-1.
@article{e8e141860cb648019fe54b8d76ddddd2,
title = "Preservation of glucose metabolism in hypertrophic GLUT4-null hearts",
abstract = "GLUT4-null mice lacking the insulin-sensitive glucose transporter are not diabetic but do exhibit abnormalities in glucose and lipid metabolism. The most striking morphological consequence of ablating GLUT4 is cardiac hypertrophy. GLUT4-null hearts display characteristics of hypertrophy caused by hypertension. However, GLUT4-null mice have normal blood pressure and maintain a normal cardiac contractile protein profile. Unexpectedly, although they lack the predominant glucose transporter in the heart, GLUT4-null hearts transport glucose and synthesize glycogen at normal levels, but gene expression of rate-limiting enzymes involved in fatty acid oxidation is decreased. The GLUT4-null heart represents a unique model of hypertrophy that may be used to study the consequences of altered substrate utilization in normal and pathophysiological conditions.",
keywords = "Glycogen, Nuclear magnetic resonance, Transport",
author = "Stenbit, {Antine E.} and Katz, {Ellen B.} and Chatham, {John C.} and Geenen, {David L.} and Factor, {Stephen M.} and Weiss, {Robert G.} and Tsao, {Tsu Shuen} and Ashwani Malhotra and Chacko, {V. P.} and Christopher Ocampo and Jelicks, {Linda A.} and Charron, {Maureen J.}",
year = "2000",
language = "English (US)",
volume = "279",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "1 48-1",

}

TY - JOUR

T1 - Preservation of glucose metabolism in hypertrophic GLUT4-null hearts

AU - Stenbit, Antine E.

AU - Katz, Ellen B.

AU - Chatham, John C.

AU - Geenen, David L.

AU - Factor, Stephen M.

AU - Weiss, Robert G.

AU - Tsao, Tsu Shuen

AU - Malhotra, Ashwani

AU - Chacko, V. P.

AU - Ocampo, Christopher

AU - Jelicks, Linda A.

AU - Charron, Maureen J.

PY - 2000

Y1 - 2000

N2 - GLUT4-null mice lacking the insulin-sensitive glucose transporter are not diabetic but do exhibit abnormalities in glucose and lipid metabolism. The most striking morphological consequence of ablating GLUT4 is cardiac hypertrophy. GLUT4-null hearts display characteristics of hypertrophy caused by hypertension. However, GLUT4-null mice have normal blood pressure and maintain a normal cardiac contractile protein profile. Unexpectedly, although they lack the predominant glucose transporter in the heart, GLUT4-null hearts transport glucose and synthesize glycogen at normal levels, but gene expression of rate-limiting enzymes involved in fatty acid oxidation is decreased. The GLUT4-null heart represents a unique model of hypertrophy that may be used to study the consequences of altered substrate utilization in normal and pathophysiological conditions.

AB - GLUT4-null mice lacking the insulin-sensitive glucose transporter are not diabetic but do exhibit abnormalities in glucose and lipid metabolism. The most striking morphological consequence of ablating GLUT4 is cardiac hypertrophy. GLUT4-null hearts display characteristics of hypertrophy caused by hypertension. However, GLUT4-null mice have normal blood pressure and maintain a normal cardiac contractile protein profile. Unexpectedly, although they lack the predominant glucose transporter in the heart, GLUT4-null hearts transport glucose and synthesize glycogen at normal levels, but gene expression of rate-limiting enzymes involved in fatty acid oxidation is decreased. The GLUT4-null heart represents a unique model of hypertrophy that may be used to study the consequences of altered substrate utilization in normal and pathophysiological conditions.

KW - Glycogen

KW - Nuclear magnetic resonance

KW - Transport

UR - http://www.scopus.com/inward/record.url?scp=0033853211&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033853211&partnerID=8YFLogxK

M3 - Article

C2 - 10899071

AN - SCOPUS:0033853211

VL - 279

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 1 48-1

ER -