PMID- 9832415 OWN - NLM STAT- MEDLINE DCOM- 19981224 LR - 20131121 IS - 0013-7227 (Print) IS - 0013-7227 (Linking) VI - 139 IP - 12 DP - 1998 Dec TI - Effects of tumor necrosis factor-alpha on glucose metabolism in cultured human muscle cells from nondiabetic and type 2 diabetic subjects. PG - 4793-800 AB - The effects of tumor necrosis factor-alpha (TNF alpha) on glucose uptake and glycogen synthase (GS) activity were studied in human skeletal muscle cell cultures from nondiabetic and type 2 diabetic subjects. In nondiabetic muscle cells, acute (90-min) exposure to TNF alpha (5 ng/ml) stimulated glucose uptake (73 +/- 14% increase) to a greater extent than insulin (37 +/- 4%; P < 0.02). The acute uptake response to TNF alpha in diabetic cells (51 +/- 6% increase) was also greater than that to insulin (31 +/- 3%; P < 0.05). Prolonged (24-h) exposure of nondiabetic muscle cells to TNF alpha resulted in a further stimulation of uptake (152 +/- 31%; P < 0.05), whereas the increase in cells from type 2 diabetics was not significant compared with that in cells receiving acute treatment. After TNF alpha treatment, the level of glucose transporter-1 protein was elevated in nondiabetic (4.6-fold increase) and type 2 (1.7-fold) cells. Acute TNF alpha treatment had no effect on the fractional velocity of GS in either nondiabetic or type 2 cells. Prolonged exposure reduced the GS fractional velocity in both nondiabetic and diabetic cells. In summary, both acute and prolonged treatment with TNF alpha up-regulate glucose uptake activity in cultured human muscle cells, but reduce GS activity. Increased skeletal muscle glucose uptake in conditions of TNF alpha excess may serve as a compensatory mechanism in the insulin resistance of type 2 diabetes. FAU - Ciaraldi, T P AU - Ciaraldi TP AD - Veterans Affairs Medical Center and Department of Medicine, University of California-San Diego, La Jolla, California 92093, USA. tciaraldi@ucsd.edu FAU - Carter, L AU - Carter L FAU - Mudaliar, S AU - Mudaliar S FAU - Kern, P A AU - Kern PA FAU - Henry, R R AU - Henry RR LA - eng GR - DK-39176/DK/NIDDK NIH HHS/United States GR - MO1-RR-00827/RR/NCRR NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, Non-P.H.S. PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Endocrinology JT - Endocrinology JID - 0375040 RN - 0 (Monosaccharide Transport Proteins) RN - 0 (Tumor Necrosis Factor-alpha) RN - 9005-79-2 (Glycogen) RN - EC 2.4.1.11 (Glycogen Synthase) RN - IY9XDZ35W2 (Glucose) SB - IM MH - Adult MH - Cells, Cultured MH - Diabetes Mellitus, Type 2/*metabolism/pathology MH - Glucose/*metabolism MH - Glycogen/biosynthesis MH - Glycogen Synthase/metabolism MH - Humans MH - Middle Aged MH - Monosaccharide Transport Proteins/metabolism MH - Muscle, Skeletal/*drug effects/*metabolism/pathology MH - Reference Values MH - Tumor Necrosis Factor-alpha/*pharmacology EDAT- 1998/12/01 00:00 MHDA- 1998/12/01 00:01 CRDT- 1998/12/01 00:00 PHST- 1998/12/01 00:00 [pubmed] PHST- 1998/12/01 00:01 [medline] PHST- 1998/12/01 00:00 [entrez] AID - 10.1210/endo.139.12.6368 [doi] PST - ppublish SO - Endocrinology. 1998 Dec;139(12):4793-800. doi: 10.1210/endo.139.12.6368.