Investigation of Fish-Based Nutrients to Protect Against Insulin Resistance in Bottlenose Dolphins (Tursiops truncatus)
Fish diets, including diets high in fish-based nutrients omega fatty acids and vitamin D3, can protect against insulin resistance, metabolic syndrome, and type 2 diabetes in humans.1-3 Like humans, dolphins can develop insulin resistance and metabolic syndrome, including elevated postprandial insulin, glucose, and triglycerides.4-6 As such, blood level differences in fish nutrients, specifically fatty acids and vitamin D, were explored between 30 dolphins with elevated (> 14 µIU/ml, n = 8) and non-elevated 2h postprandial insulin (n = 22). Dolphins with elevated insulin had higher linoleic acid (18:2n6) and oleic acid (18:1n9); and lower eicosapentaenoic acid (20:5n3), arachidonic acid (20:4n6), palmitelaidic acid (16:1), and margaric (heptadecanoic) acid (17:0) compared to dolphins with non-elevated insulin. Elevated-insulin dolphins had higher glucose, triglycerides, VLDL cholesterol, GGT, and creatinine compared to dolphins with non-elevated insulin. Linear associations were identified between margaric acid and the following: 25-hydroxyvitamin D (positive); and insulin, total iron-binding capacity, and triglycerides (negative). Interestingly, capelin and herring, common fish in managed dolphin diets, can have low to negligible arachidonic acid and margaric acid levels, compared to pinfish, a common fish of some free-ranging dolphin diets.7 The roles of margaric and arachidonic acid in dolphin metabolism warrant further exploration as potential means of treating and preventing insulin resistance and metabolic syndrome in dolphins.
The authors would like to thank the management, training, and animal care staff of the Navy Marine Mammal Program for their support of this study. We also thank Dr. Randall Wells and Dr. Kerri Slifka for kindly sharing results from their previous studies. Funding for this study was provided by the Office of Naval Research (ONR Grant Number N000141210294, IACUC #101-2012).
* Presenting author
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