Omega-3 Phospholipids from Krill Oil Enhance Intestinal Fatty Acid Oxidation More Effectively than Omega-3 Triacylglycerols in High-Fat Diet-Fed Obese Mice

Abstract

<jats:p>Antisteatotic effects of omega-3 fatty acids (Omega-3) in obese rodents seem to vary depending on the lipid form of their administration. Whether these effects could reflect changes in intestinal metabolism is unknown. Here, we compare Omega-3-containing phospholipids (krill oil; ω3PL-H) and triacylglycerols (ω3TG) in terms of their effects on morphology, gene expression and fatty acid (FA) oxidation in the small intestine. Male C57BL/6N mice were fed for 8 weeks with a high-fat diet (HFD) alone or supplemented with 30 mg/g diet of ω3TG or ω3PL-H. Omega-3 index, reflecting the bioavailability of Omega-3, reached 12.5% and 7.5% in the ω3PL-H and ω3TG groups, respectively. Compared to HFD mice, ω3PL-H but not ω3TG animals had lower body weight gain (−40%), mesenteric adipose tissue (−43%), and hepatic lipid content (−64%). The highest number and expression level of regulated intestinal genes was observed in ω3PL-H mice. The expression of FA ω-oxidation genes was enhanced in both Omega-3-supplemented groups, but gene expression within the FA β-oxidation pathway and functional palmitate oxidation in the proximal ileum was significantly increased only in ω3PL-H mice. In conclusion, enhanced intestinal FA oxidation could contribute to the strong antisteatotic effects of Omega-3 when administered as phospholipids to dietary obese mice.</jats:p>

Additive Effects of Omega-3 Fatty Acids and Thiazolidinediones in Mice Fed a High-Fat Diet: Triacylglycerol/Fatty Acid Cycling in Adipose Tissue

“…Experiments were performed similarly as before [13,19,20,39]. Thus, male C57BL/6N mice (Charles River Laboratories, Sulzfeld, Germany) were maintained at 22 • C in a 12 h light-dark cycle (light from 6.00 a.m.) with free access to water and standard chow diet (STD; 3.4% wt/wt as lipids; rat/mouse-maintenance extrudate; Ssniff Spezialdieten GmbH, Soest, Germany).…”

“…Blood glucose levels were measured by OneTouch Ultra glucometers (LifeScan, Milpitas, CA, USA), and plasma insulin levels were determined by the Sensitive Rat Insulin RIA Kit (Millipore, Billerica, MA, USA). Liver TAG content was estimated in ethanolic KOH tissue solubilisates as before [13].…”

“…Long-chain n-3 polyunsaturated fatty acids (Omega-3) in the diet, such as eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3), exert broad benefits on health (reviewed in [1][2][3][4][5]). These lipids act as natural hypolipidemics, reduce accumulation of hepatic lipids ( [6,7]; reviewed in [8]), increase plasma levels of adiponectin ([9]; reviewed in [10]), ameliorate low-grade inflammation in obesity [11] and enhance intestinal fatty acid (FA) oxidation [12,13]. Moreover, Omega-3s reduce adiposity while limiting proliferation of adipocytes in rodent models of obesity [14,15] and could reduce obesity, even in humans [16,17].…”

Krill Oil Supplementation Reduces Exacerbated Hepatic Steatosis Induced by Thermoneutral Housing in Mice with Diet-Induced Obesity

“…This is in line with our current and previous [ 29 ] results documenting the improved bioavailability of EPA at the level of liver PLs. Furthermore, a recent study on mice fed a high-fat diet based on corn oil suggests that intestinal FA oxidation, which was more effectively stimulated by krill oil compared to omega-3 PUFAs supplemented as TAGs, could also be involved in the antisteatotic effects of this marine oil [ 59 ]. It is worth mentioning that other bioactive constituents are present in krill oil, which may possess antisteatotic and insulin-sensitizing properties.…”

Advances in Technologies for Highly Active Omega-3 Fatty Acids from Krill Oil: Clinical Applications

“…Further evidence suggested that omega-3 phospholipids of krill oil enhanced intestinal fatty acid oxidation and could contribute to the anti-steatotic effects in obese mice, meaning there could exist an axis microbiota-intestine-liver [116]. Indeed, omega-3 alleviated hepatic steatosis in various rodent models of obesity even in exacerbated hepatic steatosis conditions, in which an HFD was combined with thermoneutral animal housing (i.e., ambient temperature approximately 30 • C) [117].…”