Abstract

Malnutrition is the most common presentation for California sea lions (Zalophus californiaus) at The Marine Mammal Center, which covers 600 miles of California coastline. Many die within the first few weeks of rehabilitation, and still more die weeks after admit after presumed hypoglycemic crashes. Little is known how sea lions recover from periods of severe malnutrition, as they have a drastically different diet from more commonly studied domestic animals. They are piscivores, and therefore do not consume carbohydrates, instead obtaining their glucose via gluconeogenesis in the liver.³ In addition, there may be a refeeding syndrome occurring in the emaciated animals. As studied in other species, the main refeeding electrolytes are magnesium, phosphorus, and potassium.⁴ While every animal is given electrolyte solution upon admit, individual monitoring of these electrolytes, which has been successful in other species, has never been studied.^1,5 This project aimed to better understand both the role that gluconeogenesis plays in recovery from starvation and whether survival within the first week of rehabilitation could be positively affected by implementing specific electrolyte management. The hypothesis was two-fold: that gluconeogenic enzyme activity could be measured from postmortem liver samples and that activity would be lower in animals that died of starvation, and that abnormal levels of refeeding electrolytes measured within the first week of rehabilitation of pup and yearling sea lions would be a predictor of death during rehabilitation. The records of over two thousand animals that presented from 2000 through 2011 were included in a survival analysis. Results indicated that high magnesium and phosphorus levels are significant predictors of death during rehabilitation, as well as low calcium and total protein levels. Potassium levels were not a significant predictor of death during rehabilitation. These results suggest not only that electrolyte values taken upon patient intake are significant prognostic indicators, but that monitoring and correcting electrolyte imbalances early in rehabilitation may lead to increased survival rates. To measure gluconeogenic activity in the liver, liver samples from deceased animals with varying causes of death, including malnutrition, were analyzed for the activity of the rate-limiting enzymes of gluconeogenesis: phosphoenolpyruvate carboxykinase and pyruvate carboxylase. Since this is the first study to ever measure these enzymes in sea lions, one of the goals was to establish whether they were measurable and to establish reference ranges (from animals that died for reasons that shouldn't affect the liver). The results established that these enzymes were stable after death for at least 24 hours and that they were measurable with methods very similar to those established for other species.² While more samples are needed to draw any conclusions, very preliminary results do not suggest a deficit in gluconeogenic enzymes in animals that died of malnutrition. Further studies should be implemented to explore how glucose is metabolized in these animals and why they go into hypoglycemic shock. Results from both parts of this study highlight the need for more research on glucose metabolism and malnutrition in California sea lions and the possible opportunities for treatment of a devastating condition.

Acknowledgements

The authors wish to thank: Dr. Kevork Hagopian of UC Davis, School of Veterinary Medicine, Department of Molecular Biosciences for his aid in laboratory work; volunteers and staff at The Marine Mammal Center for mentorship, access to medical records, and help in collecting samples; Dr. Philip Kass of the Department of Epidemiology at UC Davis, School of Veterinary Medicine for his statistics expertise; and Morris Animal Foundation and UC Davis School of Veterinary Medicine Students Training in Advanced Research for their generous funding.

References

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