Effect of in vivo injection of cholera and pertussis toxin on glucose transport in rat skeletal muscle
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Effect of in vivo injection of cholera and pertussis toxin on glucose transport in rat skeletal muscle. / Ploug, Thorkil; Han, X; Petersen, L N; Galbo, H.
I: American Journal of Physiology (Consolidated), Bind 272, Nr. 1 Pt 1, 01.1997, s. E7-17.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Effect of in vivo injection of cholera and pertussis toxin on glucose transport in rat skeletal muscle
AU - Ploug, Thorkil
AU - Han, X
AU - Petersen, L N
AU - Galbo, H
PY - 1997/1
Y1 - 1997/1
N2 - Cholera toxin (CTX) and pertussis toxin (PTX) were examined for their ability to inhibit glucose transport in perfused skeletal muscle. Twenty-five hours after an intravenous injection of CTX, basal transport was decreased approximately 30%, and insulin- and contraction-stimulated transport was reduced at least 86 and 49%, respectively, in both the soleus and red and white gastrocnemius muscles. In contrast, PTX treatment was much less efficient. Impairment of glucose transport appeared to develop 10-15 h after CTX administration, which coincided with development of hyperglycemia despite hyperinsulinimia, increased plasma free fatty acid levels, increased adenosine 3',5'-cyclic monophosphate (cAMP) concentrations in muscle, but no difference in plasma catecholamines. Twenty-five hours after CTX treatment, GLUT-4 protein in both soleus and red gastrocnemius muscles was decreased, whereas no change in GLUT-1 protein content was found. In contrast, GLUT-4 mRNA was unchanged, but transcripts for GLUT-1 were increased > or = 150% in all three muscles from CTX-treated rats. The findings suggest that CTX via increased cAMP impairs basal as well as insulin- and contraction-stimulated muscle glucose transport, at least in part from a decrease in intramuscular GLUT-4 protein.
AB - Cholera toxin (CTX) and pertussis toxin (PTX) were examined for their ability to inhibit glucose transport in perfused skeletal muscle. Twenty-five hours after an intravenous injection of CTX, basal transport was decreased approximately 30%, and insulin- and contraction-stimulated transport was reduced at least 86 and 49%, respectively, in both the soleus and red and white gastrocnemius muscles. In contrast, PTX treatment was much less efficient. Impairment of glucose transport appeared to develop 10-15 h after CTX administration, which coincided with development of hyperglycemia despite hyperinsulinimia, increased plasma free fatty acid levels, increased adenosine 3',5'-cyclic monophosphate (cAMP) concentrations in muscle, but no difference in plasma catecholamines. Twenty-five hours after CTX treatment, GLUT-4 protein in both soleus and red gastrocnemius muscles was decreased, whereas no change in GLUT-1 protein content was found. In contrast, GLUT-4 mRNA was unchanged, but transcripts for GLUT-1 were increased > or = 150% in all three muscles from CTX-treated rats. The findings suggest that CTX via increased cAMP impairs basal as well as insulin- and contraction-stimulated muscle glucose transport, at least in part from a decrease in intramuscular GLUT-4 protein.
KW - Animals
KW - Biological Transport
KW - Catecholamines
KW - Cholera Toxin
KW - Cyclic AMP
KW - Glucose
KW - Glucose Transporter Type 1
KW - Glucose Transporter Type 4
KW - Injections, Intravenous
KW - Insulin
KW - Male
KW - Monosaccharide Transport Proteins
KW - Muscle Contraction
KW - Muscle Proteins
KW - Muscle, Skeletal
KW - Pertussis Toxin
KW - RNA, Messenger
KW - Rats
KW - Rats, Wistar
KW - Virulence Factors, Bordetella
M3 - Journal article
C2 - 9038845
VL - 272
SP - E7-17
JO - American Journal of Physiology - Cell Physiology
JF - American Journal of Physiology - Cell Physiology
SN - 0363-6143
IS - 1 Pt 1
ER -
ID: 123665900