Feeding Different Omega-3 Polyunsaturated Fatty Acid Sources Influences Renal Fatty Acid Composition, Inflammation, and Occurrence of Nephrocalcinosis in Female Sprague-Dawley Rats

Abstract

<p class="MsoNormal"> The general population is encouraged to increase omega-3 polyunsaturated fatty acid (n-3 PUFA) intake in order to optimize health for preventative health care. Consumers are typically unaware that different amounts, types, and structural forms of n-3 PUFA have different efficacy. Therefore, the objectives of this study were to characterize different sources of n-3 PUFAs and to determine whether consumption of these oils influences renal fatty acid composition and renal health. Lipid classes and fatty acid profile of corn (CO), flaxseed (FO), menhaden (MO), salmon (SO), tuna (TO) or krill (KO) oils were determined by thin-layer and gas chromatography. All dietary oils consisted of >65% triglyceride with the exception of KO. KO and FO also contained phospholipids. FO was rich in the n-3 PUFA, alpha-linolenic acid (18:3n-3) whereas, the marine oils were rich in the long-chain n-3 PUFAs (>18 carbons). Following characterization of the oil sources, female Sprague-Dawley rats (age 28 d) were randomly assigned (n = 10/group) to be fed a high fat 12% (wt) diet consisting of these different oil sources for 8 weeks. Rats fed MO, TO, and SO had significantly higher renal eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3) deposition and this in turn, modulated inflammatory responses. Feeding rats MO, SO and TO reduced urinary excretion of 13,14-dihydro-15-keto prostaglandin E₂. Feeding rats TO and SO reduced (<em>P</em> ≤ 0.002) nuclear factor kappa B activity and circulating TNF<em>α</em> (<em>P</em> < 0.05). In contrast, rats consuming KO had heavier kidney weights (<em>P</em> < 0.001), total calcium content, and histological evidence of renal calcification and tubulo-interstitial injury. This was due to increased (<em>P</em> < 0.001) urinary phosphorus excretion associated with the phospholipids content of KO. The study results indicated that consumption of n-3 PUFAs influences renal health and the effects varied depending on the n-3 PUFA source consumed. </p

Dietary omega-3 PUFA improved tubular function after ischemia induced acute kidney injury in mice but did not attenuate impairment of renal function

“…Overall, feeding of the STD+n3 diet led to a massive elevation of absolute and relative levels of n3-PUFA (18:4n3, 20:4n3, 20:5n3, 22:5n3, 22:6n3) with simultaneous decrease in n6-PUFA (18:3n6, 20:2n6, 20:3n6, 20:4n6, 22:4n6, 22:5n6) in the circulation and in the kidney. These changes are in line with previous reports showing extensive modulation of PUFA composition in blood compartments and tissues by n3-PUFA feeding [22,[55][56][57][58][59] or by endogenous n3-PUFA accumulation in transgenic fat-1 mice [22,55,60]. Compared to the STD chow, in response to the STD+n3 feeding the relative content of the main long-chain PUFA ARA, EPA and DHA in the kidney changed from 16.4% to 8.6% (0.5 fold), 0.04% to 4.1% (99 fold) and 10.1% to 21.0% (2 fold), respectively.…”

“…Compared to the STD chow, in response to the STD+n3 feeding the relative content of the main long-chain PUFA ARA, EPA and DHA in the kidney changed from 16.4% to 8.6% (0.5 fold), 0.04% to 4.1% (99 fold) and 10.1% to 21.0% (2 fold), respectively. Similar alterations in the renal fatty acid composition were also observed in mice and rats fed chow containing 1-3% each EPA and DHA (in each case in almost equal amount) [22,[56][57][58]. Relative levels in the kidney in response to STD+n3 are similar to earlier findings for n3-PUFA feeding in rodents ranging for EPA from 1-4.6% in mice and from 5.2-9.7% in rats and for DHA from 6.7-24.6% in mice and from 5.5-7.8% in rats depending primarily on the diet composition (e.g.…”

A reexamination of krill oil bioavailability studies

“…KO di- and tri-glycerides can vary from about 13 to 34% and non-esterified fatty acids can vary from 3.5 to as much as 36%. A report of a third commercial KO source indicates that it is composed of only 16% phospholipid, 24% triglyceride and 60% of a “polar, non-phospholipid fraction [ 18 ] which is composed mainly of cholesterol, mono- and diglycerides and red pigment, mainly astaxanthin” [ 19 ]. Thus two of the three commercial KO preparations had phospholipids as a minor component.…”

“…There has been a recent animal study that has raised some concern about possible KO kidney toxicity [ 18 ]. In this study KO was compared to several fish oils (menhaden (MO), salmon (SO) and tuna (TO)) as well as a flaxseed oil (FO) and a corn oil (CO) control after feeding to 4 wk old rats for a subsequent 8 wks as a 12% fat diet.…”

Krill Products: An Overview of Animal Studies

“…Expression levels of key enzymes in β-oxidation and lipogenesis were different after KO feeding for 8 weeks, compared to placebo, which ultimately led to decreased fasting blood glucose and improved glucose tolerance in the rabbits. However, when the KO administered is outside of the 5% NOAEL at a level of 11.8% of the diet, then the rats supplemented for 8 weeks showed significantly higher kidney weights, total calcium content, and renal calcification and tubulo-interstitial injury compared to the control group [ 33 ]. Authors have suggested that the reason might be the higher urinary phosphorus excretion due to the phospholipid content of KO.…”