Abstract
The rate of glucose metabolism has been shown to be correlated to glucose uptake in swimbladder gas gland cells. Therefore, it is assumed that in the European eel silvering, i.e., the preparation of the eel for the spawning migration to the Sargasso Sea, coincides with an enhanced capacity for glucose uptake. To test this hypothesis expression of all known glucose transport proteins has been assessed at the transcript level in yellow and in silver eels, and we also included Anguillicola crassus infected swimbladders. Glucose uptake by rete mirabile endothelial cells could be crucial for the countercurrent exchange capacity of the rete. Therefore, this tissue was also included in our analysis. The results revealed expression of ten different members of the slc2 family of glucose transporters, of four slc5 family members, and of kiaa1919 in gas gland tissue. Glucose transporters of the slc2 family were expressed at very high level, and slc2a1b made up about 80% of all slc2 family members, irrespective of the developmental state or the infection status of the eel. Overall, the slc5 family contributed to only about 8% of all detected glucose transport transcripts in gas gland tissue, and the slc2 family to more than 85%. In rete capillaries, the contribution of sodium-dependent glucose transporters was significantly higher, leaving only 66% for the slc2 family of glucose transporters. Neither silvering nor the infection status had a significant effect on the expression of glucose transporters in swimbladder gas gland tissue, suggesting that glucose metabolism of eel gas gland cells may not be related to transcriptional changes of glucose transport proteins.
Highlights
Gas secretion in the swimbladder is dependent on glucose metabolism, resulting in the production of lactic acid in the glycolytic pathway, and of CO2, generated in the pentose phosphate shunt (Pelster and Scheid 1993; Walsh and Milligan 1993; Pelster et al 1994; Pelster 1995b)
A comparison of transcript levels of glucose transport proteins GLUT1-4 in various tissues of Atlantic cod Gadus morhua revealed that the GLUT1 transport protein is expressed in most tissues examined, and glut1 expression accounted for 97.6% of the glucose transporter transcripts in gas gland tissue (Hall et al 2014)
Using the primer sets designed on the basis of the eel genome, we obtained the expected amplicons for all glucose transport family members except slc2a1a, slc2a9, and slc5a2
Summary
Gas secretion in the swimbladder is dependent on glucose metabolism, resulting in the production of lactic acid in the glycolytic pathway, and of CO2, generated in the pentose phosphate shunt (Pelster and Scheid 1993; Walsh and Milligan 1993; Pelster et al 1994; Pelster 1995b). Along the partial pressure gradient, CO2 diffuses from gas gland cells into the swimbladder, contributing by about 20% to newly secreted gas (Kobayashi et al 1990), and into the blood, causing an acidification of the blood during passage of the gas gland cells. The acidification of the blood during passage of the gas gland tissue switches on the Root effect, so that oxygen is released from the hemoglobin and diffuses into the swimbladder along the partial pressure gradient (Pelster and Weber 1991; Pelster and Randall 1998; Pelster 2001). In gas gland tissue glut expression was several fold higher than in other tissues (brain, heart, red blood cells), and the elevated level of glut transcript expression in gas gland cells coincided with an elevated rate of glucose consumption, as determined from 3H2O production from labeled glucose (Hall et al 2014). A recent detailed study on glucose metabolism in gas gland tissue of the Atlantic cod confirmed the critical importance of the GLUT1 transport protein for the rate of glucose utilization (Clow et al 2016)
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