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
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
复制标题
膳食中添加加热亚麻籽粒增加羊绒山羊皮下脂肪组织中n-3长链多不饱和脂肪酸浓度的机制
DOI:
10.1093/jas/sky386
复制
发表时间:
2019
影响因子:
3.3
通讯作者:
Yan Sumei
中科院分区:
文献类型:
--
作者:
Wang Xue;Martin Graeme B;Liu Shulin;Shi Binlin;Guo Xiaoyu;Zhao Yanli;Yan Sumei
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.