The mechanism through which dietary supplementation with heated linseed grain increases n-3 long-chain polyunsaturated fatty acid concentration in subcutaneous adipose tissue of cashmere kids

Abstract

The aim of this study was to investigate the effects of dietary supplementation with heated linseed on the fatty acid (FA) composition of the plasma, liver, and subcutaneous adipose tissue (SADT) of Albas white cashmere kids, particularly the effect on n-3 long-chain polyunsaturated FA profiles and the mRNA expression of genes related to lipid metabolism in SADT. Sixty 4-month-old castrated male kids (average BW 18.6 ± 0.1 kg) were selected and randomly allocated into three groups in a randomized block design. Three dietary treatments were used: (1) basal diet without supplementation (Control), (2) basal diet supplemented with linseed oil (LSO), and (3) basal diet supplemented with heated linseed grain (HLS). The diets were fed for 104 d, consisting of 14 d for adaptation followed by 90 d of measurement. Different FA profiles were found in SADT between LSO and HLS. Kids fed HLS had more C18:3n3 (P < 0.0001), C22:6n3 (P = 0.007), and n-3 PUFA (P < 0.0001) and a less (P < 0.0001) n-6/n-3 ratio than LSO kids. These FA differences between LSO and HLS kids were due to the increased expression of elongation of very long chain FA protein 5 (P < 0.0001), delta-6 desaturase (P < 0.0001), and peroxisome proliferator-activated receptor α (P = 0.003) in SADT of HLS kids and was also associated with liver fat metabolism. Together, these results suggest that the consumption of HLS leads to more C22:6n3 than LSO in SADT by increasing liver C22:6n3 content and by increasing SADT mRNA expression of ELOVL5 and FADS2 through promoting PPARα expression.

Figure 1.

Schema illustrating our current understanding of the ways in which the addition of heated linseed grain (HLS) affects the flows and synthesis of n-3 long-chain polyunsaturated fatty acids (FAs) in cashmere goats. Black solid arrows are used where the effect of HLS was greater than the effect of LSO (both greater than control values). Black broken arrows and grey solid arrows are used where the effects of HLS and LSO did not differ significantly (but both greater than control values). Grey broken arrows indicate hypothetical changes (not measured). PPARα = peroxisome proliferator-activated receptor alpha; FADS1 = delta-5 desaturase; FADS2 = delta-6 desaturase; ELOVL5 = elongation of very long chain FAs protein 5; ACOX1 = acyl-coenzyme A oxidase 1; SLC27A2 = solute carrier family 27 member; CD36 = FA translocase/CD36. For the sake of clarity, only the pathways that show clear responses to linseed treatment are shown: for example, FADS1, ACOX1 are not affected in SADT or liver by either LSO or HLS. Other components of FA pathways are also omitted because they were not tested in the present study: elongation of very long chain FAs protein 2; Enoyl-Coenzyme A, hydratase/3-hydroxyacyl Co A deshydrogenase; Sterol-carrier protein 2; 2,4-dienoyl coA reductase 2 and 3-oxoacyl-Coenzyme A thiolase.