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Endocrinology Vol. 139, No. 12 4793-4800
Copyright © 1998 by The Endocrine Society

ARTICLES

Effects of Tumor Necrosis Factor-{alpha} on Glucose Metabolism in Cultured Human Muscle Cells from Nondiabetic and Type 2 Diabetic Subjects1

Theodore P. Ciaraldi, Leslie Carter, Sunder Mudaliar, Philip A. Kern and Robert R. Henry

Veterans Affairs Medical Center and Department of Medicine (0673), University of California-San Diego (T.P.G., L.C., S.M., R.R.H.), La Jolla, California 92093; and the Veterans Affairs Medical Center and Department of Medicine, University of Arkansas for Medical Sciences (P.A.K.), Little Rock, Arkansas 72205

Address all correspondence and requests for reprints to: Dr. Theodore P. Ciaraldi, Department of Medicine (0673), University of California-San Diego, La Jolla, California 92093. E-mail: tciaraldi{at}ucsd.edu

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.




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