EFFECTS OF DIETARY LINOLENATE ON ARACHIDONATE
EFFECTS OF DIETARY LINOLENATE ON ARACHIDONATE
批准号:
3242793
负责人:
DANIEL H HWANG
金额:
$4.06万
依托单位国家:
美国
项目类别:
财政年份:
1989
资助国家:
美国
项目状态:
已结题
起止时间:
1989-06-01 至 1992-05-31
关键词:
alkanes arachidonate collagen dietary lipid eicosanoid metabolism laboratory rat leukotrienes linolenate lipoxygenase macrophage nutrition related tag omega 3 fatty acid phospholipids platelet activation platelet aggregation prostaglandin endoperoxide synthase radioimmunoassay thromboxanes unsaturated fatty acids
中文摘要
这项研究的目的是评估膳食营养素的功效。
亚麻酸(18:3 n-3),与二十碳五烯酸(20:5 n-3)相比,或
二十二碳六烯酸(22:6 n-3),其在鱼油中丰富,以抑制
花生四烯酸(20:4 n-6)在大鼠体内形成类花生酸
组织中 20:5 n-3在降低
血栓形成的可能性被认为主要是由于其
竞争性抑制20:4 n-6转化为血栓烷A2
(TXA 2),并通过置换降低血小板中的20:4 n-6水平。
一个重要的问题是,另一种类型的饮食是否
n-3脂肪酸可以达到类似或甚至更有益的效果,
20:5n-3。 本申请人提出,膳食18:3 n-3抑制
将亚油酸(18:3 n-6)转化为20:4 n-6。 它还抑制了
形成20:4 n-6的环加氧酶衍生产物。 此外,委员会认为,
18:3 n-3不是白三烯(LT)的底物,而20:5 n-3是白三烯的底物。
导致五烯形成的5-脂氧合酶的优选底物
LTS. 因此,膳食18:3 n-3可能是比20:5 n-3更有效的抑制剂。
3为LT的生物合成。 具体的目的是比较18:3 n-3与
20:5 n-3或22:6 n-3对类二十烷酸前体水平的影响
游离脂肪酸级分和组织磷脂中的脂肪酸,和(2)
在组织中形成20:4 n-6和20:5 n-3来源的类二十烷酸。
大鼠将在24小时内喂食分级量的纯化的18:3 n-3、20:5 n-3或22:6 n-3。
持续12周存在恒定量的18:2n-6。 花生酸
将通过放射免疫测定法测定组织中合成的
免疫层析测定。 长远目标是建立
我们饮食中的n-3与n-6脂肪酸的理想比例,以减少某些
冠心病的风险。 目前,大多数饮食指南使用
多不饱和脂肪酸(PUFA),不区分PUFA类型
(n-3或n-6)。 今后,这一比例可能需要在
饮食指南。
英文摘要
The objective of the proposed study is to evaluate the efficacy of dietary
linolenic acid (18:3n-3), as compared to eicosapentaenoic acid (20:5n-3) or
docosahexaenoic acid (22:6n-3) which are abundant in fish oil, to inhibit
the formation of eicosanoids derives from arachidonic acid (20:4n-6) in rat
tissues. The suggested beneficial effects of 20:5n-3 in reducing
thrombogenic potential are considered to be primarily due to its
competitive inhibition of the conversion of 20:4n-6 to thromboxane A2
(TXA2), and reduction of the 20:4n-6 level in platelets by displacement.
An important question can be raised as to whether another type of dietary
n-3 fatty acid can achieve similar or even more beneficial effects than
20:5n-3. This applicant proposes that dietary 18:3n-3 inhibits the
conversion of linoleic acid (18:3n-6) to 20:4n-6. It also inhibits the
formation of cyclooxygenase-derived products of 20:4n-6. Furthermore,
18:3n-3 is not a substrate for leukotrienes (LT), whereas 20:5n-3 is a
preferred substrate for 5-lipoxygenase leading to the formation of pentaene
LTs. Thus, dietary 18:3n-3 may be a more effective inhibitor than 20:5n-
3 for the biosynthesis of LTs. The specific aim is to compare 18:3n-3 with
20:5n-3 or 22:6n-3 for its effects on: (1) levels of eicosanoid precursor
acids in free fatty acid fractions and tissue phospholipids, and (2) the
formation of eicosanoids derived both from 20:4n-6 and 20:5n-3 in tissues.
Rats will be fed graded amounts of purified 18:3n-3, 20:5n-3 or 22:6n-3 in
the presence of a constant amount of 18:2n-6 for 12 weeks. Eicosanoids
synthesized in tissues will be determined by radioimmunoassay and
immunochromatographic assay. The long term objective is to establish the
desirable ratio of n-3 to n-6 fatty acids in our diets to reduce certain
risks of coronary heart disease. Presently, most dietary guidelines use
polyunsaturated fatty acids (PUFA) without differentiating types of PUFA
(n-3 or n-6). In the future, this ratio may need to be specified in the
dietary guidelines.
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海外基金