ACTH1-24 stimulates muscle cell glucose uptake.
3H-2-deoxyglucose (2-DG) uptake was measured in L6A-1 rat skeletal muscle cells (a rapidly fusing subclone of L6), following addition of several concentrations (10(-16) to 10(-9)M) of the N-terminal fragment of ACTH1-24 to cells deprived of serum and insulin for 21 hours, but maintained in the presence of (5 micrograms/ml) insulin (stimulated state). There was a marked dose-dependent increase of 2-DG uptake at the various ACTH1-24 (P less than 0.001). There was no correlation between the time of exposure of the cells to serum-free conditions and the rate of uptake of 2-DG at the various ACTH1-24 concentrations both in the basal and insulin-stimulated states. Addition of catochalasin B (50 microM) to the cells, which inhibited both basal and insulin-stimulated uptake of 2-DG (by 70% and 91%, respectively) completely eliminated the enhancement of both of these uptake rates to 10(-12)M ACTH1-24. The results suggest that: 1) ACTH1-24 stimulates carrier-mediated uptake of glucose in skeletal muscle cells. 2) The site of action of ACTH1-24 is on the non-insulin mediated glucose uptake (NIMGU) system. 3) ACTH1-24 may be a useful probe to delineate some of the events associated with the NIMGU pathway.
Levin
P A
PA
Department of Pediatrics, University of Maryland School of Medicine, Baltimore.
Bistritzer
T
T
Hanukoglu
L
L
Max
S R
SR
Roeder
L M
LM
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002460:Cell Line; D003366:Cosyntropin / Q000494:pharmacology*; D003571:Cytochalasin B / Q000494:pharmacology; D003847:Deoxyglucose / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology; D007700:Kinetics; D009132:Muscles / Q000187:drug effects / Q000378:metabolism*
D007328:Insulin; D003366:Cosyntropin; D003571:Cytochalasin B; D003847:Deoxyglucose