Abstract

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 (p > 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.

Highlights

  • Obesity is highly prevalent nowadays, being responsible for several comorbidities such as type-2 diabetes, hypertension, and cardiovascular diseases [1]

  • Values obtained for peroxide value (PV), p-anisidine value (AV) and total oxidation (TOTOX) (0.29 ± 0.01, 3.70 ± 0.33 and 3.99 ± 0.34, respectively) revealed low lipid oxidation development, which agrees with previous research on different kinds of fish oils, including salmon oil [16,17,18,19]

  • deodorized refined salmon oil (DSO) fatty acid composition and quantification revealed that the main fatty acids were oleic acid (C18:1 n-9), linoleic acid (C18:2 n-6), palmitic acid (C16:0); docosahexaenoic acid (C22:6 n-3, DHA); eicosapentaenoic acid (C20:5 n-3, EPA) with 38.90 ± 0.02, 14.68 ± 0.16, 11.40 ± 0.23, 3.57 ± 0.12 and 3.50 ± 0.06 g/100 g total fatty acids, respectively (Table 1)

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Summary

Introduction

Obesity is highly prevalent nowadays, being responsible for several comorbidities such as type-2 diabetes, hypertension, and cardiovascular diseases [1]. This pathophysiological condition is characterized by a lower level of systemic inflammation [2] and leads to an increase in basal proinflammatory mediators which affects the adequate insulin response in tissues such as skeletal. Dietary intake of omega-3 fatty acids produces a reduction in insulin resistance due to their effect on the expression and activity of enzymes that metabolize glucose, decreasing the expression of lipogenic enzymes and increasing the β-oxidation of fatty acids (FA) or the anti-inflammatory effect [10,11]. The anti-inflammatory actions of (C20:5 n-3, EPA) and (C22:6 n-3, DHA) are crucial in the reported preventive mechanism

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