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Glucose Transporter in Insulin Sensitive Tissues of Lean and Obese Mice. Effect of the Thermogenic Agent BRL 26830A^*

Institut National dé la Sante et de la Recherche Médicale U145, Faculte de Medecine, Nice, France

Address requests for reprints to: Dr. Y. Le Marchand-Brustel, INSERM U 145, Faculte de Médecine, Avenue de Valombrose, 06034 Nice Cédex, France.

Abstract

Glucose transport is decreased in skeletal muscle and adipose tissues of obese, hyperglycemic, insulin-resistant animals. Here we have characterized the glucose transporter(s) in muscle and adipose tissues from normal and obese mice, and we have studied the effect of a treatment with the thermogenic agent BRL 26830A.

Glucose transporters were examined in crude tissue membrane fractions (microsomal + plasma membranes) by Western blot analysis using antipeptide antibodies specific for the erythroid (Glut 1) or muscle/fat (Glut 4) glucose transporters. In these insulin sensitive tissues, only Glut 4 was detected. In membranes from obese animals, the Glut 4 number was decreased by 40% ± 4% in brown adipose tissue (mean ± SEM of 9 preparations, P < 0.001), whether the results were expressed per total tissue or per mg of protein. By contrast, Glut 4 number was unchanged in skeletal muscle. In white adipose tissue of obese animals, Glut 4 number per total fat pad was increased. However, due to the enlarged fat pad size, Glut 4 content was diminished when expressed per mg of white adipose tissue membrane protein in obese compared to lean animals.

After a 18 day-treatment with BRL 26830A (1 or 2 mg/kgday), glycemia of obese mice, which was slightly elevated compared to lean animals, was normalized, while insulinemia remained markedly above control values. In brown adipose tissue, the total number of Glut 4 returned to normal at 1 mg of the drug, or increased by 63% ± 14% at 2 mg. Since membrane protein content was increased by the treatment, when results were expressed per mg of membrane protein, Glut 4 was similar in lean and BRL 26830A (1 or 2 mg) treated obese mice. BRL 26830A treatment did not modify Glut 4 in skeletal muscle, and it increased Glut 4 number in white adipose tissue in a dosedependent manner. In conclusion, in obese mice, the glucose transporter number was reduced mainly in brown adipose tissue, a defect which could contribute to the hyperglycemic syndrome. Treatment with the thermogenic agent BRL 26830A normalized in parallel glycemia and glucose transporter number in brown adipose tissue, suggesting that this tissue could play a role in glucose homeostasis in rodents. (Endocrinology 127: 2687–2695, 1990)

Footnotes

^* This work was supported by grants from the French Association for the Study of Myopathy (AFM), Institut National de la Sante et de la Recherche Medicale, France, the Region Provence-Alpes-Cote d’Azur, and the University of Nice, France. Christine Olichon-Berthe is the recipient of a fellowship from the French Association for the Study of Myopathy (AFM). Nathalie Rochet was the recipient of a fellowship from the Fondation pour la Recherche Medicale (Paris, France).

Received April 23, 1990.

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