Preservation of glucose metabolism in hypertrophic GLUT4-null hearts.
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.
Stenbit
A E
AE
Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York 10461-1602, USA.
Katz
E B
EB
Chatham
J C
JC
Geenen
D L
DL
Factor
S M
SM
Weiss
R G
RG
Tsao
T S
TS
Malhotra
A
A
Chacko
V P
VP
Ocampo
C
C
Jelicks
L A
LA
Charron
M J
MJ
D000818:Animals; D001794:Blood Pressure; D006332:Cardiomegaly / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D003847:Deoxyglucose / Q000378:metabolism; D003971:Diastole; D005260:Female; D005947:Glucose / Q000378:metabolism*; D051275:Glucose Transporter Type 4; D006973:Hypertension / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009004:Monosaccharide Transport Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D009124:Muscle Proteins; D009206:Myocardium / Q000473:pathology*; D012727:Sex Characteristics
D051275:Glucose Transporter Type 4; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; C495693:Slc2a4 protein, mouse; D003847:Deoxyglucose; D005947:Glucose