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Department of Medicine, Division of Endocrinology, University of Arkansas for Medical Sciences, and The John L. McClellan VA Medical Center (S.R., P.A.K.), Little Rock, Arkansas 72205; and Veterans Administration Medical Center and Department of Medicine (T.P.C., R.R.H., S.M.), University of California, San Diego, California 92023
Address all correspondence and requests for reprints to: Philip A. Kern, M.D., Associate Chief of Staff-Research, John L. McClellan Memorial Veterans Hospital, 4300 West 7th Street, Little Rock, Arkansas 72205. E-mail: kernphilipa{at}exchange.uams.edu
The effect of leptin on glucose transport, lipogenesis, and lipoprotein lipase activity was studied in cultured rat adipocytes and 3T3-L1 adipocytes. Leptin had no effect on basal and insulin stimulated glucose transport in isolated adipocytes from the rat and the genetically obese mouse. The incorporation of glucose into lipids was also unaffected. Lipoprotein lipase (LPL) activity remained unchanged in response to leptin in these cells, as well as in minced adipose tissue. Leptin also had no effect on both basal and insulin-stimulated glucose transport in cultured rat and human skeletal muscle cells. These studies showed that leptin had no effect on glucose transport, lipoprotein lipase activity, and insulin action in fat and muscle cells in vitro.
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