Abstract
Fatty acids released from adipose triacylglycerol stores by lipolysis provide vertebrates with an important source of energy. We investigated the role of microsomal triacylglycerol hydrolase (TGH) in the mobilization of adipocyte triacylglycerols through inactivation of the TGH activity by RNA interference or chemical inhibition. Attenuation of TGH activity resulted in decreased basal but not isoproterenol-stimulated efflux of fatty acids from 3T3-L1 adipocytes. Lack of TGH activity was accompanied by accumulation of cellular triacylglycerols and cholesteryl esters without any changes in the expression of enzymes catalyzing triacylglycerol synthesis (diacylglycerol acyltransferases 1 and 2) or degradation (adipose triglyceride lipase and hormone-sensitive lipase). Inhibition of TGH-mediated lipolysis also did not affect insulin-stimulated Glut4 translocation from intracellular compartments to the plasma membrane or glucose uptake into adipocytes. These data suggest that TGH plays a role in adipose tissue triacylglycerol metabolism and may be a suitable pharmacological target for lowering fatty acid efflux from adipose tissue without altering glucose import.
Highlights
Obesity is a chronic disease with increasing prevalence in most of the world but in Western countries [1]
Insulin action mediates TG deposition, and when energy is required, free fatty acids are liberated from TG stores by lipolysis and carried by serum albumin in the plasma for delivery to tissues for utilization [41, 42]
Because TG hydrolase (TGH) is expressed in the adipose tissue [17,18,19], we hypothesized that TGH may be involved in the mobilization of fat depots and may contribute to plasma free fatty acid levels
Summary
We show that TGH does not co-localize with Glut in 3T3-L1 adipocytes in either basal or insulin-stimulated conditions and that inhibition of TGH-catalyzed TG lipolysis in 3T3-L1 adipocytes does not prevent insulin-stimulated Glut translocation from intracellular compartment to plasma membrane or insulin-stimulated glucose uptake in intact cells
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