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    • Such responses have led to the idea

    2022-01-15

    Such responses have led to the idea that elasmobranchs may be glucose intolerant. However, certain species, such as the North Pacific spiny dogfish (Squalus suckleyi; note that the species used in this study was previously referred to as Squalus acanthias but a study by Ebert et al. (2010) provided evidence that the Atlantic and Pacific populations are in fact two separate species and suggested we revert to the former name of Squalus suckleyi) feed on molluscs and crustaceans which can consist of up to 25% fasudil synthesis (Jones and Geen, 1977). In addition, the rectal gland, which is activated following the consumption of food, has been shown to be glucose-dependent (Walsh et al., 2006) and as such it is important to understand how glucose is transported and metabolised in this group of fishes. Furthermore, elasmobranchs appeared early in the vertebrate lineage and thus understanding the mechanisms of glucose uptake in this group of fish would provide valuable insights into the evolution of glucoregulation in vertebrates. As with elasmobranchs, teleosts have also been considered glucose intolerant, given the time it takes to clear a glucose load in comparison to mammals (5–36h; reviewed by Moon (2001) and Polakof et al. (2012)) although some species, such as the American eel (Anguilla rostrate) and black bullhead catfish (Ameiurus melas), were able to restore plasma glucose levels within 60min of injection (Legate et al., 2001). Species that have been deemed glucose intolerant, however, still tend to exhibit mammalian-like responses to hyperglycaemia. For instance, Blasco et al. (1996) showed that injecting brown trout (Salmo trutta) with glucose caused an increase in plasma insulin levels as well as 3- and 4-fold increases in glucose uptake by red and white skeletal muscle, respectively. Similarly, rainbow trout (Oncorhynchus mykiss) limited the hyperglycaemia experienced during constant glucose infusions through increased uptake and excretion (Choi and Weber, 2015). These authors also determined that the glucose infusions completely inhibited hepatic glycogenolysis and gluconeogenesis which occurs in mammals in response to insulin. Typically, an increase in plasma glucose concentration is accompanied by the release of insulin which stimulates the transport of previously synthesised GLUT 1 and 4 proteins from intracellular storage vesicles to the plasma membrane of myocytes to enhance glucose uptake (Calderhead et al., 1990, Huang and Czech, 2007). Furthermore, insulin causes an increase in both GLUT1 (Walker et al., 1989) and GLUT4 (Bourey et al., 1990) protein and mRNA levels in mammalian skeletal muscle cells. In rainbow trout skeletal muscle, insulin induced a significant increase in both glut1 and 4 mRNA levels (Diaz et al., 2009) and GLUT4 protein levels (Diaz et al., 2007), similar to the effects observed in mammals. In mammalian adipocytes, insulin is typically believed to induce GLUT translocation as is the case in skeletal muscle, however, there are conflicting reports in vitro. For instance, GLUT4 protein and mRNA have been shown to increase in response to insulin in some studies with no changes in GLUT1 (see review by Pessin and Bell, 1992) but in other studies, GLUT4 protein and mRNA decreased while GLUT1 protein and mRNA increased in response to insulin (Flores-Riveros et al., 1993, Sargeant and Paquet, 1993). These discrepancies may be due to the conditions under which the adipocytes were allowed to differentiate or the length of the insulin treatment period. Very little work has been done on glucose transporters in elasmobranchs, likely due to their presumed “glucose intolerance.” Indeed, the delayed responses to insulin and glucose injections led Anderson et al. (2002) to suggest that elasmobranchs altogether lack the insulin-responsive GLUT4 (as was once the belief in teleosts). This may not be the case, however, as a prior study by Deck et al. (2016) identified sequences for GLUTs 1, 3, and 4 in elasmobranchs and observed increases in glut4 mRNA levels in the muscle, liver, and intestine in S. suckleyi in response to feeding. These changes were believed to be due to the actions of insulin and although this does not provide definitive evidence for a functional GLUT4 protein, similar responses are observed in response to insulin in mammals and teleosts as outlined above.