Functional redundancy of glucose acquisition mechanisms in the hindgut of Pacific hagfish (Eptatretus stoutii).

This study examined the mechanisms of glucose acquisition in the hindgut of Pacific hagfish (Eptatretus stoutii) using in vitro gut sac techniques. The intestine was determined to have the capacity to digest maltose into glucose along the entirety of the tract, including the foregut. Glucose uptake was biphasic and consisted of a high-affinity, low-capacity concentration-dependent component conforming to Michaelis-Menten kinetics (K 0.37mM, J 8.48nmol/cm/h) as well as a diffusive component. There was no observed difference in glucose flux rate along the length of the intestine, similar to other nutrients investigated in the hagfish intestine. A reduced sodium (<1mM) environment did not result in a change in glucose uptake rates, likely due to a functional redundancy of glucose transporters. There was no observed effect of phloretin, yet the sodium glucose-linked transporter (SGLT)-specific inhibitor phlorizin significantly reduced glucose uptake at all concentrations tested (0.0001-1mM). Additionally, the glucose transporter (GLUT) inhibitor cytochalasin b significantly reduced glucose transport rates. The effects of these pharmacological inhibition experiments suggest the presence of multiple types of glucose transport proteins. This study clarifies the uptake strategies used by hagfish to acquire glucose at the intestine and provides insight into the evolution of such transport systems in early-diverging vertebrates.