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    • In the present study a

    2021-11-24

    In the present study, a significant increase in liver glut4 mRNA levels as well as an increase in liver glycogen content was observed in the dogfish in response to glucose-loading, although we did not observe any changes in liver glycogen content or glut mRNA levels following insulin administration and as circulating levels of insulin cannot currently be measured in elasmobranchs, it is difficult to determine if the observed responses were the direct action of increases in plasma insulin concentration. In this study, however, bovine insulin was used as there is currently no dogfish insulin available and Patent (1970) showed that bovine insulin is less potent in the S. acanthias (5Ukg−1 of bovine insulin was required to achieve the same decrease in plasma 2-Arachidonoyl Glycerol as 0.3Ukg−1 of dogfish insulin, the latter dose being similar to what was used in the present study). Interestingly, increases in glycogen synthase and glut4 mRNA levels were observed in the muscle in response to both insulin and glucose-loading and thus it is likely that insulin is a factor responsible for increasing glut transcription in elasmobranch muscle. Further, as the decreases in plasma glucose observed during the insulin experiment were minor, it is possible that insulin does affect glycogen metabolism but either the dose or the use of a heterologous insulin did not increase glucose uptake sufficiently to stimulate glycogen deposition. Alternatively, alterations in fuel usage or metabolic rate could be responsible for the lack of increase in glycogen content but such parameters were not examined in this study. Clearly there is a need to synthesise elasmobranch insulin and develop an antibody for the measurement of this hormone in elasmobranch fish.
    Conclusions The data presented here suggest that dogfish are in fact capable of glucoregulating, albeit at a slower rate relative to mammals, and our data suggest that they may use mechanisms similar to those described in mammals and teleosts, with alterations in glycogen synthesis and glut mRNA levels, suggesting conservation of these mechanisms throughout the vertebrate lineage. This finding is not entirely surprising as it has been shown that the insulin receptor is functionally much more conserved in vertebrates than insulin itself (Muggeo et al., 1979). Despite the lack of tools available to gain a complete understanding of insulin and its role in glucose regulation in elasmobranchs (homologous hormones or assays and the ability to perform receptor binding studies), we have shown with the addition of molecular expression of key glucose transport proteins that elasmobranchs are likely quite capable of mounting a insulinotropic response that may be mechanistically similar to what has been described in other vertebrate groups.
    Acknowledgments Many thanks to Dr. Eric Clelland of the Bamfield Marine Sciences Centre for ensuring that the experiments ran smoothly; to Alyssa Weinrauch, Alexander Clifford, and Rachel Munger for their assistance with sampling; and to John Planes for providing the dogfish. This research was funded by an NSERC Discovery Grant to PJW, who is also supported by the Canada Research Chair Program.
    Main Text Glucose is the major energy fuel of the central nervous system. However, its availability is restricted given the selective permeability of the blood brain barrier (BBB) and the relative lack of carbohydrate stores in the brain. Thus, glucose transport across the BBB and into neural cells is critical for cerebral physiologic function and energy metabolism (for a review, see Chen et al.). GLUT1 is the key regulator of glucose across the BBB. The importance of this process is illustrated by the observation that dominant mutations in SLC2A1 (OMIM: 138140), which encodes GLUT1, cause epilepsy with variable degrees of intellectual disability (ID) and/or movement disorder. Once glucose enters the brain’s extracellular space, it is taken up by different cerebral cells through various glucose transporters, which are expressed in developmentally and cell-type-specific manners. Whether disruption of these neural glucose transporters also causes neurodevelopment disorders remains unknown.