Pinealectomy causes glucose intolerance and decreases adipose cell responsiveness to insulin in rats

• Published in: American journal of physiology: endocrinology and metabolism 1998-12, Vol.275 (6), p.E934-E941
• Main Authors: Lima, Fabio B, Machado, Ubiratan F, Bartol, Ione, Seraphim, Patricia M, Sumida, Doris H, Moraes, Solange M. F, Hell, Naomi S, Okamoto, Maristela M, Saad, Mario J. A, Carvalho, Carla R. O, Cipolla-Neto, Jose
• Format: Article
• Language: English
• ISSN: 0193-1849; 1522-1555
• DOI: 10.1152/ajpendo.1998.275.6.e934

1  Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, 05508-900 Sao Paulo; and 2  Department of Clinics, School of Medicine, State University of Campinas, 13081-970 Sao Paulo, Brazil Although the pineal gland influences several physiological systems, only a few studies have investigated its role in the intermediary metabolism. In the present study, male Wistar rats, pinealectomized or sham-operated 6 wk before the experiment, were submitted to both intravenous glucose tolerance tests (IVGTT) and insulin binding as well as glucose transport assays in isolated adipocytes. The insulin receptor tyrosine kinase activity was assessed in liver and muscle. The insulin secretory response during the IVGTT was impaired, particularly in the afternoon, and the glucose transport responsiveness was 33% lower in pinealectomized rats. However, no difference was observed in the insulin receptor number of adipocytes between groups as well as in insulin-stimulated tyrosine kinase activity, indicating that the initial steps in the insulin signaling were well conserved. Conversely, a 40% reduction in adipose tissue GLUT-4 content was detected. In conclusion, pinealectomy is responsible for both impaired insulin secretion and action, emphasizing the influence of the pineal gland on glucose metabolism. pineal gland; glucose transport; GLUT-4; insulin receptor tyrosine kinase; adipocytes