EPA/DHA Concentrate by Urea Complexation Decreases Hyperinsulinemia and Increases Plin5 in the Liver of Mice Fed a High-Fat Diet

• Main Authors: Alejandra Espinosa, Andrés Ross, Gretel Dovale-Rosabal, Francisco Pino-de la Fuente, Ernesto Uribe-Oporto, Camila Sacristán, Paulina Ruiz, Rodrigo Valenzuela, Nalda Romero, Santiago P. Aubourg, Alicia Rodríguez
• Format: Article
• Language: English
• Published: MDPI AG 2020-07-01
• Series: Molecules
• Subjects: deodorized refined salmon oil; urea complexation; EPA + DHA concentration; metabolic alterations; insulin; obesity
• Online Access: https://www.mdpi.com/1420-3049/25/14/3289

<b>: </b>Dietary intake of eicosapentaenoic/docosahexaenoic acid (EPA/DHA) reduces insulin resistance and hepatic manifestations through the regulation of metabolism in the liver. Obese mice present insulin resistance and lipid accumulation in intracellular lipid droplets (LDs). LD-associated proteins perilipin (Plin) have an essential role in both adipogenesis and lipolysis; Plin5 regulates lipolysis and thus contributes to fat oxidation. The purpose of this study was to compare the effects of deodorized refined salmon oil (DSO) and its polyunsaturated fatty acids concentrate (CPUFA) containing EPA and DHA, obtained by complexing with urea, on obesity-induced metabolic alteration. CPUFA maximum content was determined using the Box–Behnken experimental design based on Surface Response Methodology. The optimized CPUFA was administered to high-fat diet (HFD)-fed mice (200 mg/kg/day of EPA + DHA) for 8 weeks. No significant differences (<i>p</i><i> </i>> 0.05) in cholesterol, glycemia, LDs or transaminase content were found. Fasting insulin and hepatic Plin5 protein level increased in the group supplemented with the EPA + DHA optimized product (38.35 g/100 g total fatty acids) compared to obese mice without fish oil supplementation. The results suggest that processing salmon oil by urea concentration can generate an EPA+DHA dose useful to prevent the increase of fasting insulin and the decrease of Plin5 in the liver of insulin-resistant mice.