Alterations in adipocyte glucose transporter GLUT4 and circulating adiponectin and visfatin in rat adjuvant induced arthritis.

Unlabelled: Rheumatoid arthritis in humans brings about impaired insulin sensitivity and glucose tolerance. Since adipose tissue plays a role in glucose homeostasis, we evaluated the size of adipocytes, the amount of glucose transporter type 4 (GLUT4) in adipocyte plasma membranes, and circulating insulin, glucose, and adipokines affecting glucose metabolism, resistin, adiponectin and visfatin during experimental adjuvant arthritis (AA) in male Lewis rats. AA was induced by a single injection of complete Freund's adjuvans. Adipocyte diameter was assessed microscopically, GLUT4 was measured by Western blotting. Plasma insulin, adiponectin, visfatin were quantitated by RIA, and resistin by ELISA. Arthritic rats showed cachexia, reduced adipocyte size, and downregulated membrane GLUT4 (4065 +/- 962 vs. 9911 +/- 680 arb. units of optic density, p < 0.01), reduced plasma adiponectin (1.956 +/- 0.10 vs. 3.16 +/- 0.22 microg/ml, p < 0.001), and enhanced visfatin (1.84 +/- 1.05 vs. 1.24 +/- 0.1 ng/ml, p < 0.01). Plasma glucose and insulin were unaltered, as were the resistin levels.

Conclusion: AA induced cachexia results in reduction of adipocyte size, and paradoxically also in downregulation of GLUT4 in adipocyte membranes. This is supposed to be functionally related to the reduced adiponectin levels. The upregulated visfatin in rat arthritis is a novel finding, and it confirms its role in autoimmunity across the species.