Fluorodeoxyglucose uptake and glucose transporter expression in experimental inflammatory lesions and malignant tumours: effects of insulin and glucose loading.
The expression of glucose transporters (GLUTs) and its relationship to fluorodeoxyglucose accumulation in malignant tumours have been well investigated, while such a relation has not been studied in inflammatory lesions. The aim of the present study was to investigate the effects of insulin and glucose loading on the expression of GLUTs in inflammatory lesions and compare them with those in malignant tumours in relation to fluorodeoxyglucose accumulation. All tissue specimens used in this study were obtained in our previous study, in which rats were inoculated with allogenic hepatoma cells (KDH-8), Staphylococcus aureus, or turpentine oil into the left calf muscle and divided into three subgroups: insulin loaded, glucose loaded, and control groups. The expression of glucose transporters (GLUT-1 to GLUT-5) was investigated by immunostaining the lesions (n=5-6, for each group). In all control groups, the expression levels of GLUT-1 and GLUT-3 were significantly higher than those of GLUT-2, GLUT-4 and GLUT-5. Insulin loading did not significantly affect the expression levels of GLUT-1 and GLUT-3 in these lesions except for a significant but slight decrease in the GLUT-1 expression level in the inflammatory lesion of non-infectious origin (89% of the control value). Glucose loading significantly decreased the expression level of GLUT-1 in the inflammatory lesion of non-infectious origin (70% of the control value, P<0.01), and that of GLUT-3 in the inflammatory lesion of infectious origin (70% of the control value, P<0.05), while the expression levels of GLUT-1 and GLUT-3 in the tumour were not significantly affected. These results demonstrate the effects of insulin and glucose loading on the expression level of a molecule (GLUT proteins). The decreased GLUT-1 and GLUT-3 expression levels induced by glucose loading may partly explain the impaired FDG uptake observed in our previous study.
Zhao
S
S
Department of Nuclear Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Kuge
Y
Y
Tsukamoto
E
E
Mochizuki
T
T
Kato
T
T
Hikosaka
K
K
Nakada
K
K
Hosokawa
M
M
Kohanawa
M
M
Tamaki
N
N
D000818:Animals; D019788:Fluorodeoxyglucose F18 / Q000493:pharmacokinetics*; D005947:Glucose / Q000378:metabolism* / Q000494:pharmacology; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000378:metabolism; D007249:Inflammation / Q000000981:diagnostic imaging / Q000378:metabolism; D007328:Insulin / Q000378:metabolism* / Q000494:pharmacology; D008114:Liver Neoplasms, Experimental / Q000000981:diagnostic imaging* / Q000378:metabolism*; D008297:Male; D009004:Monosaccharide Transport Proteins / Q000145:classification / Q000378:metabolism*; D011817:Rabbits; D011877:Radionuclide Imaging; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D051381:Rats; D017208:Rats, Wistar; D012680:Sensitivity and Specificity; D013203:Staphylococcal Infections / Q000000981:diagnostic imaging / Q000378:metabolism
D007004:Hypoglycemic Agents; D007328:Insulin; D009004:Monosaccharide Transport Proteins; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18; D005947:Glucose