The effect of glucose on lipolytic regulation was studied in isolated human adipocytes. Glucose enhanced adipocyte glycerol release in the presence and absence of the β-adrenergic agent ritodrine by 150–200% of control rates. The glucose effect was maximal at just >1 mM glucose and could not be attributed to prevention of a time-dependent decline in lipolysis. Glucose not only increased lipolytic stimulation at each of several concentrations of ritodrine but also enhanced the sensitivity to stimulation at low concentrations of the agent. Ritodrine-stimulated lipolysis was inhibited by insulin by 50–60%; although glucose increased absolute rates of lipolysis, it did not affect the relative inhibition of lipolysis by insulin or the sensitivity to the hormone. In investigating a possible cause of the glucose effect on lipolysis, it was found that the addition of adenosine deaminase increased lipolytic rates in the absence of glucose and blunted the relative stimulation of lipolysis by glucose, the latter implicating extracellular adenosine in the mechanism of the glucose effect.
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Original Contributions|
July 01 1986
Potentiation by Glucose of Lipolytic Responsiveness of Human Adipocytes
Colette Moussalli;
Colette Moussalli
Division of Endocrinology and Metabolism, Department of Medicine, Medical College of Virginia, Virginia Commonwealth University
Richmond, Virginia
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Robert W Downs;
Robert W Downs
Division of Endocrinology and Metabolism, Department of Medicine, Medical College of Virginia, Virginia Commonwealth University
Richmond, Virginia
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James M May
James M May
Division of Endocrinology and Metabolism, Department of Medicine, Medical College of Virginia, Virginia Commonwealth University
Richmond, Virginia
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Address reprint requests to Dr. James M. May, Box 111, MCV Station, Richmond, VA 23298.
Diabetes 1986;35(7):759–763
Article history
Received:
August 20 1985
Revision Received:
December 31 1985
PubMed:
3721062
Citation
Colette Moussalli, Robert W Downs, James M May; Potentiation by Glucose of Lipolytic Responsiveness of Human Adipocytes. Diabetes 1 July 1986; 35 (7): 759–763. https://doi.org/10.2337/diab.35.7.759
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