|D'agord Schaan, Beatriz|
Submitted to: Metabolism
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/20/2006
Publication Date: 8/20/2006
Citation: Zanquetta, M.M., Nascimento, M.E.C., Mori, R.C.T., D'Agord Schaan, B., Young, M.E., Machado, U.F. 2006. Participation of beta-adrenergic activity in modulation of GLUT4 expression during fasting and refeeding in rats. Metabolism. 55(11):1538-1545. Interpretive Summary: When someone does not eat, a number of things happen in the body to help prevent the sugar in your blood from decreasing too much. If the sugar in your blood decreases too much, then you die. This also becomes a problem when diabetics inject themselves with too much insulin. The purpose of our study was to find out if adrenaline helps prevent the sugar in the blood from decreasing too much when not eating. The results show that adrenaline plays an important role in regulating the use of glucose by several organs when rats are not allowed to eat. This work is important for improving our understanding of how our body prevents blood sugar from decreasing too much when we don't eat.
Technical Abstract: Through in vitro studies, several factors have been reported as modulators of GLUT4 gene expression. However, the role(s) of each potential GLUT4 modulator is not completely understood in the in vivo setting. The present study has investigated the hypothesis that beta-adrenergic stimulation participates in modulation of GLUT4 expression during fasting and refeeding. As such, GLUT4 messenger RNA (mRNA) and protein were investigated in insulin-sensitive tissues during a 48-hour fast. In addition, the effects of 8-hour refeeding on GLUT4 mRNA in the gastrocnemius muscle and interscapular brown adipose tissue (BAT) were investigated. Whether beta-adrenoceptor blockade by propranolol (20 mg/kg) treatment influenced the responsiveness to fasting/refeeding was also investigated. The results show that fasting repressed GLUT4 gene and protein expression in BAT, white adipose tissue, and soleus muscle, but had no effect on the gastrocnemius muscle. Refeeding induced a rapid overexpression of GLUT4 mRNA in both gastrocnemius (approximately 25%, P < .05) and BAT (approximately 200%, P < .001). Propranolol treatment induced an increase (approximately 60%, P < .05) in GLUT4 mRNA at the end of the fasting period. In contrast, propranolol treatment attenuated GLUT4 mRNA induction after refeeding; the latter may be due to attenuation of postprandial insulin levels. These results suggest that sympathetic activity is important for the repression of GLUT4 gene expression during fasting. In contrast, sympathetic control of the GLUT4 gene seems to be overbalanced by metabolic/hormonal modulators during refeeding stage. Taken together, the results suggest that feeding behavior influences GLUT4 gene expression pattern through changes in sympathetic activity, especially during long-term starvation periods.