EFFECTS OF DIETARY LINOLENATE ON ARACHIDONATE
EFFECTS OF DIETARY LINOLENATE ON ARACHIDONATE
批准号:
3242796
负责人:
DANIEL H HWANG
金额:
$4.13万
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
建议的研究目的是评估饮食的疗效。
亚麻酸(18:3n-3),与二十碳五烯酸(20:5n-3)或
鱼油中富含二十二碳六烯酸(22:6N-3),可抑制
花生四烯酸(20:4n-6)在大鼠体内形成二十碳二烯
纸巾。20:5N-3在减量中的有益效果
血栓形成的可能性被认为主要是由于它的
竞争性抑制20:4N-6向血栓素A2的转化
(TXA2),并通过置换降低血小板中20:4N-6水平。
一个重要的问题是,另一种饮食是否
N-3脂肪酸可以达到类似甚至更有益的效果
20:5N-3。本申请者建议饮食18:3n-3抑制
亚油酸(18:3N-6)转化为20:4N-6。它还抑制了
20:4N-6环氧合酶衍生产物的形成。此外,
18:3n-3不是白三烯(LT)的底物,而20:5n-3是
5-脂氧合酶形成并戊烯的首选底物
这就是。因此,饮食18:3n-3可能是一种比20:5n-3更有效的抑制剂。
3为LTS的生物合成。具体目的是将18:3n-3与
20:5n-3或22:6n-3对:(1)二十烷类前体水平的影响
游离脂肪酸组分和组织磷脂中的酸,以及(2)
组织中20:4n-6和20:5n-3来源的二十烷类化合物的形成。
分别以18:3n-3、20:5n-3或22:6n-3的纯化量饲喂大鼠
恒定量18:2N-6存在12周。二十烷类化合物
在组织中合成的将通过放射免疫分析和
免疫层析法。我们的长远目标是建立
我们饮食中n-3和n-6脂肪酸的理想比例可以减少某些
患冠心病的风险。目前,大多数饮食指南使用
不区分多不饱和脂肪酸类型的多不饱和脂肪酸
(n-3或n-6)。将来,此比率可能需要在
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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