PMID: 7016868Jun 25, 1981Paper

Energy-dependent and protein synthesis-independent recycling of the insulin-sensitive glucose transport mechanism in fat cells.

The Journal of Biological Chemistry
T KonoT L Blevins

Abstract

The glucose transport mechanism of rat epididymal fat cells was reconstituted into egg lecithin liposomes, and their carrier-mediated transport activity ws estimated from the difference in the rates of uptake of D-[3H]glucose and L-[14C]glucose. Insulin increased the glucose transport activity in the plasma membrane-rich fraction while decreasing the activity in the Golgi-rich fraction in agreement with our previous data (Suzuki, K., and Kono, T. (1980) Proc. Natl. Acad. Sci. U. S. A. 77, 2542-2545). The development of the insulin effects was inhibited when cells were exposed to 2,4-dinitrophenol or KCN before the insulin treatment. In addition, the reversal of the insulin effects was blocked upon exposure of insulin-treated cells to 2,4-dinitrophenol or KCN prior to the elimination of the hormone. In contrast, neither development nor reversal of the insulin effects was affected by cycloheximide or puromycin. The temperature coefficients of the transport activities reconstituted from the basal or insulin-treated forms of the plasma membrane-rich or Golgi-rich fractions were all identical. The recoveries of protein, 5'-nucleotidase, UDP-galactose:N-acetylglucosamine galactosyltransferase, and NADH dehydrogenase into subcellular ...Continue Reading

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