Reversion of Hyperferritinemia and Metabolic Syndrome in Bottlenose Dolphins (Tursiops truncatus) Associated with Increased Dietary Margaric Acid (C17:0)
IAAAM 2015
Stephanie K. Venn-Watson1*; Celeste Parry1; Mark Baird1; Sasha Stevenson1; Kevin Carlin1; Risa Daniels1; Cynthia R. Smith1; Richard Jones2; Randall Wells3; Eric D. Jensen4
1National Marine Mammal Foundation, San Diego, CA, USA; 2Kennedy Krieger Institute, Baltimore, MD, USA; 3Chicago Zoological Society c/o Mote Marine Laboratory, Sarasota, FL, USA; 4U.S. Navy Marine Mammal Program, San Diego, CA, USA

Abstract

Similar to humans, there is evidence that wild and managed care bottlenose dolphins can develop metabolic syndrome (elevated insulin, glucose, and triglycerides) and associated hyperferritinemia. While fish diets and fish-based fatty acids may protect against metabolic syndrome in humans, study findings have been inconsistent. In our study, higher percent serum margaric acid (C17:0), a saturated fatty acid found in mullet and pinfish but not capelin, independently predicted lower insulin in dolphins. Further, dolphins with percent serum C17:0 less than 0.4% of total fatty acids were more likely to have elevated insulin (greater than 14 μIU/ml) compared to dolphins with higher C17:0. As such, our hypothesis was that increased dietary intake of C17:0 would result in lower insulin. Diets of six dolphins were modified by weight (maintaining the same kilocalories) to 25% capelin, 25% pinfish and/or mullet, and 50% herring, mackerel, and/or squid and fed daily for 24 weeks. This modified diet increased the average daily dietary intake of C17:0 from 400 mg to 1,700 mg. Two-hour postprandial blood samples (following ingestion of 1/3 of the daily diet) were collected at weeks 0, 3, 12, 18, and 24. During the feeding study, C17:0 increased in both serum and erythrocyte membranes; high ferritin reversed; and metabolic syndrome indices normalized toward reference levels within six months. These effects were not found in four control dolphins. These data are preliminary, and expanded feeding studies are underway with more dolphins at the Navy Marine Mammal Program to better understand the role of C17:0 and other fatty acids on dolphin metabolism.

Acknowledgements

U.S. Patent Pending, Serial No. 14/591,660. The authors would like to thank the management, training, and animal care staff of the Navy Marine Mammal Program, Space and Naval Warfare Systems Center Pacific for their support of this study; as well as Dr. Laura Kienker from the Office of Naval Research. This study was funded by ONR, Grant Number N000141210294, IACUC Animal Care and Use Protocol #101-2012.

* Presenting author

  

Speaker Information
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Stephanie K. Venn-Watson
National Marine Mammal Foundation
San Diego, CA, USA


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