Bioconversion of α-linolenic acid to n-3 LCPUFA and expression of PPAR-alpha, acyl coenzyme A oxidase 1 and carnitine acyl transferase I are incremented after feeding rats with α-linolenic acid-rich oils

Abstract

High dietary intake of n-6 fatty acids in relation to n-3 fatty acids may generate health disorders, such as cardiovascular and other chronic diseases. Fish consumption rich in n-3 fatty acids is low in Latin America, it being necessary to seek other alternatives to provide α-linolenic acid (ALA), precursor of n-3 LCPUFA (EPA and DHA). Two innovative oils were assayed, chia (Salvia hispanica) and rosa mosqueta (Rosa rubiginosa). This study evaluated hepatic bioconversion of ALA to EPA and DHA, expression of PPAR-α, acyl-Coenzyme A oxidase 1 (ACOX1) and carnitine acyltransferase I (CAT-I), and accumulation of EPA and DHA in plasma and adipose tissue in Sprague-Dawley rats. Three experimental groups were fed 21 days: sunflower oil (SFO, control); chia oil (CO); rosa mosqueta oil (RMO). Fatty acid composition of total lipids and phospholipids from plasma, hepatic and adipose tissue was assessed by gas-liquid chromatography and TLC. Expression of PPAR-α (RT-PCR) and ACOX1 and CAT-I (Western blot). CO and RMO increased plasma, hepatic and adipose tissue levels of ALA, EPA and DHA and decreased n-6:n-3 ratio compared to SFO (p < 0.05, One-way ANOVA and Newman-Keuls test). CO increased levels of ALA and EPA compared to RMO (p < 0.05). No significant differences were observed for DHA levels. CO also increased the expression of PPAR-α, ACOX1 and CAT-I. Only CAT-I levels were increased by RO. CO and RMO may be a nutritional alternative to provide ALA for its bioconversion to EPA and DHA, and to increase the expression of PPAR-α, ACOX1 and CAT-I, especially CO-oil.

Silkworm pupae powder ingestion increases fat metabolism in swim-trained rats

“…In contrast to what was suggested in the AMPK results, this was believed to be thanks to the intake of silkworm pupae which are rich in unsaturated fatty acids. In other words, it was reported that the 4 week-long treatment of unsaturated fatty acids to rats increased the level of PPAR-α [30] by a significant degree, which could be explained by a report that claimed that the α-linoleic acid enhanced the appearance rate of the PPAR-α [31,32]. Especially, the silkworm pupae powder intake control group which did not exercise also showed an increased appearance rate of the PPAR-α, which was thought to be a meaningful result.…”

Combination of low dose major n3 PUFAs in fresh water mussel lipid is an alternative of EPA–DHA supplementation in inflammatory conditions of arthritis and LPS stimulated macrophages

“…Contribution of high ALA and SDA in the 54.73% of unsaturated fatty acids present in LMLF was an interesting finding, as these n3 fatty acids play critical role in de novo synthesis of long chain n3 fatty acids [28]. These fatty acids have clinically proven antiinflammatory activities [29][30][31].…”

Estrogen and n-3 polyunsaturated fatty acid supplementation have a synergistic hypotriglyceridemic effect in ovariectomized rats

“…Indeed, n-3 PUFA supplementation has been shown to increase expression of PPARa, p-AMPK, and CPT1 in liver or/and skeletal muscle of rats (Gonzalez-Manan et al 2012;Motawi et al 2009). In line with these results, the present study showed that n-3 PUFA supplementation up-regulated the expression of PPARa, CPT1, p-AMPK, and AMPK in liver and/ or skeletal muscle of OVX rats.…”

“…In several studies, n-3 PUFA supplementation suppressed the synthesis of fatty acids and TG by reducing hepatic expression of the sterol regulatory element-binding protein 1 (SREBP1), acetyl-CoA carboxylase 1 (ACC1), fatty acid synthase (FAS), and diacylglycerol acyltransferase 2 (DGAT2) (Lu et al 2011;Sekiya et al 2003;Harris and Bulchandani 2006). Additionally, n-3 PUFA supplementation accelerated b-oxidation by increasing expression of peroxisome proliferator-activated receptor (PPAR) a, carnitine palmitoyltransferase 1 (CPT1), and adenosine monophosphate-activated protein kinase (AMPK) in liver and/or skeletal muscle (Gonzalez-Manan et al 2012;Hardie et al 2012;Suchankova et al 2005).…”