Glucose Kinetics in Yearling California Sea Lions (Zalophus californianus)
IAAAM 2012
Vanessa A. Fravel1; William Van Bonn1; Frances Gulland1; Carlos Rios1; Peter J. Havel2
1The Marine Mammal Center, Fort Cronkhite, Sausalito, CA, USA; 2Department of Molecular Biosciences, School of Veterinary Medicine, and Department of Nutrition, University of California, Davis, CA, USA

Abstract

The Marine Mammal Center (TMMC) cares for many malnourished California sea lion (CSL) (Zalophus californianus) yearlings every year.1 One of the common sequelae to malnutrition in young California sea lions is hypoglycemia. Clinical signs of hypoglycemia can vary from lethargy to seizures. Administering glucose during a hypoglycemic crisis is vital to treating the animal. Furthermore, premature removal from glucose supplementation can cause a recurrence of severe hypoglycemia and often death.5 Traditional veterinary approaches to hypoglycemia treatment involve the use of intravenous or oral dextrose supplementation. These treatment options can be easily accomplished in many terrestrial animals, but marine mammals pose therapeutic and diagnostic difficulties as vascular access and catheter maintenance can be extremely difficult. Neither CSL milk nor their prey contain any simple sugars; therefore, adverse side effects, such as diarrhea, often accompany oral dextrose treatment.2 This study investigates serum glucose kinetics after different routes of dextrose administration.

California sea lion yearlings were used in this study when they were ready for release from rehabilitation and were clinically healthy. Six groups of animals consisting of two sea lions each were treated with one of the following treatments: intravenous dextrose, subcutaneous dextrose, intraperitoneal dextrose, oral dextrose, oral blended herring and water or nothing (control, no treatment or feeding). All groups were given the same dose of 500 mg/kg of dextrose. Each sea lion was fasted overnight, then placed under isoflurane anesthesia to facilitate ultrasound-guided jugular catheter (16 G x 15 cm) placement. Once the catheter was placed, a time zero blood sample was taken, then dextrose was administered as defined by the group the animal was in. Blood samples (6 ml) were then collected at times 5, 15, 30, 60, 120, 180, 240 minutes. The animal was maintained under isoflurane anesthesia until the 30-minute blood sample was collected. All of the subsequent samples were taken under physical restraint via the jugular catheter. Blood was immediately placed into EDTA and serum separator tubes and then centrifuged within 10 minutes of collection. Serum was used to measure glucose values within 15 minutes with an Alfa Wasserman Vet Ace chemistry analyzer. The plasma obtained from the EDTA tubes was frozen at -80°C, and levels of insulin, glucagon, and cortisol were determined by RIA at UC Davis. After the last blood sample was taken at 240 minutes, the catheter was removed. No adverse effects of catheter placement were observed.

Intravenous and IP dextrose elevated blood glucose for three hours and were associated with a serum insulin peak at 60 min post dextrose infusion. Fasting blood glucose values in all the animals tested ranged from 126–209 mg/dL, and fasting insulin values ranged from 2.8–17.5 µU/ml. These values appear more consistent with bottlenose dolphin (Tursiops truncatus) fasting insulin values than those in humans or domestic dogs.3,4 Results from this project provide insight into California sea lion glucose tolerance, glucose metabolism under general anesthesia, and provide useful information that will potentially help in the treatment of hypoglycemic, malnourished California sea lions.

Acknowledgements

We thank James Graham from the University of California at Davis for all of his hard work completing the insulin, glucagon, and cortisol assays. We would also like to thank Lauren Campbell, Dr. Sophie Dennison, Deb Wickham, Jen Soper, and all of the volunteers that helped make this project a success.

References

1.  Greig DG, Gulland FMD, Kreuder C. A decade of live California sea lion (Zalophus californianus) strandings along the central California coast: causes and trends, 1991–2000. Aquat Mamm. 2005;31:11–22.

2.  Heath CB. California, Galapagos, and Japanese sea lions, Zalophus californianus, Z. wollebaeki, and Z. japonicus. In: Perrin W, ed. Encyclopedia of Marine Mammals. San Francisco, CA: Elsevier; 2008:170–176.

3.  Martinez FJ, Rizza RA, Romero JC. High-fructose feeding elicits insulin resistance, hyperinsulinism, and hypertension in normal mongrel dogs. Hypertens J Am Heart Assoc. 1994;23:456–463.

4.  Venn-Watson S, Carlin K, Ridgway S. Dolphins as animal models for type 2 diabetes: sustained, post-prandial hyperglycemia and hyperinsulinemia. Gen Comp Endocrinol. 2011;170:193–199.

5.  Walsh MT, Gearhart S. Intensive care. In: Dierauf LA, Gulland FMD, eds. CRC Handbook of Marine Mammal Medicine. New York, NY: CRC Press; 1979:689–700.

  

Speaker Information
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Vanessa A. Fravel
The Marine Mammal Center
Fort Cronkhite
Sausalito, CA, USA


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