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Thiazolidinediones Inhibit Lipoprotein Lipase Activity In Adipocytes, Subramanian Ranganathan, Philip A. Kern
Thiazolidinediones Inhibit Lipoprotein Lipase Activity In Adipocytes, Subramanian Ranganathan, Philip A. Kern
Clinical and Translational Science Faculty Publications
The thiazolidinediones troglitazone and BRL 49653 improve insulin sensitivity in humans and animals with insulin resistance. Adipose tissue lipoprotein lipase is an insulin-sensitive enzyme. We examined the effects of thiazolidinediones on lipoprotein lipase expression in adipocytes. When added to 3T3-F442A, 3T3-L1, and rat adipocytes in culture, troglitazone and BRL 49653 inhibited lipoprotein lipase activity. This inhibition was observed at concentrations as low as 0.1 μM and within 2 h after addition of the drug. Lipoprotein lipase activity was inhibited in differentiated adipocytes as well as the differentiating cells. Despite this decrease in enzyme activity, these drugs increased mRNA levels in …
Effects Of Tumor Necrosis Factor-Α On Glucose Metabolism In Cultured Human Muscle Cells From Nondiabetic And Type 2 Diabetic Subjects, Theodore P. Ciaraldi, Leslie Carter, Sunder Mudaliar, Philip A. Kern, Robert R. Henry
Effects Of Tumor Necrosis Factor-Α On Glucose Metabolism In Cultured Human Muscle Cells From Nondiabetic And Type 2 Diabetic Subjects, Theodore P. Ciaraldi, Leslie Carter, Sunder Mudaliar, Philip A. Kern, Robert R. Henry
Clinical and Translational Science Faculty Publications
The effects of tumor necrosis factor-a (TNFα) 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 TNFα (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 TNFα 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 TNFα 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 TNFα treatment, the level of glucose transporter-1 protein was elevated in nondiabetic (4.6-fold increase) and type 2 (1.7-fold) cells. Acute TNFα 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 TNFα up-regulate glucose uptake activity in cultured human muscle cells, but reduce GS activity. Increased skeletal muscle glucose uptake in conditions of TNFα excess may serve as a compensatory mechanism in the insulin resistance of type 2 diabetes.