ライフサイエンスコーパス: n-6 fatty acid

1 of n-3 fatty acids (absolute and relative to n-6 fatty acids).

2 n the western diet there is an oversupply of n-6 fatty acids.

3 APOA5 interactions were specific for dietary n-6 fatty acids.

4 t sesamin inhibited Delta(5)-desaturation of n-6 fatty acids.

5 s derived from arachidonic acid (AA), a 20:4(n-6) fatty acid.

6 ur knowledge, the first to indicate that the n-6 fatty acid AdA effectively blocks production of LTB(

7 er risk, there is experimental evidence that n-6 fatty acids, again via eicosanoid production, may en

8 n plasma phospholipid proportions of n-3 and n-6 fatty acids [alpha-linolenic acid (ALA), EPA, docosa

9 By way of lipoxygenase products, n-6 fatty acids also regulate expression of the invasive

10 c increase in the ingestion of saturated and n-6 fatty acids and concomitant decrease in n-3 fatty ac

11 ting an association between intake of n-3 or n-6 fatty acids and leukocyte telomere length (LTL) in m

12 sociation between dietary saturated, n-3 and n-6 fatty acids and PD risk.

13 The H3-L6 and H3 diets altered n-3 and n-6 fatty acids and several of their nociceptive oxylipi

14 onsible for increases in the ratio of n-3 to n-6 fatty acids and the ratio of long-chain n-3 to n-6 f

15 in fish oil--from the more abundant omega-6 (n-6) fatty acids and so they must rely on a dietary supp

16 ntake of linoleic acid (LA), the predominant n-6 fatty acid, and coronary heart disease (CHD) risk ha

17 -3 fatty acids, a detrimental effect of high n-6 fatty acids, and the possible importance of the rati

18 food label include health effects of n-3 and n-6 fatty acids; appropriate labeling of trans fatty aci

19 rated from arachidonic acid (polyunsaturated n-6 fatty acid) by the enzyme 5-lipoxygenase.

20 a-linolenic acid added to a diet enriched in n-6 fatty acids can effectively substitute for fish oil-

21 tal cancer or overall major chronic disease; n-6 fatty acid consumption did not influence these relat

22 Higher n-6 fatty acid consumption has also been hypothesized to

23 fibre, total polyunsaturated, total n-3 and n-6 fatty acid contents increased linearly (p<0.05) by r

24 ous pools of 18:2n6 and 18:3n3 indicate that n-6 fatty acid conversion rates are greater than those o

25 These results suggest that n-6 fatty acids do not inhibit the antiinflammatory effe

26 In contrast, combining DHA with n-6 fatty acids, either arachidonic acid or docosapentae

27 rage oil, respectively), as compared with an n-6 fatty acid-enriched diet (corn oil) on the following

28 djustment for individual circulating n-3 and n-6 fatty acids, except arachidonic acid.

29 Dietary intake of the n-6 fatty acid (FA) linoleic acid (LA) has a strong grow

30 ween the dietary intake and ratio of n-3 and n-6 fatty acids (FAs) and DES occurrence.

31 y recalls, we estimated the ratios of n-3 to n-6 fatty acids for both highly unsaturated fatty acids

32 our diets and can be classified in 2 groups: n-6 fatty acids found in plant seeds and n-3 fatty acids

33 n increased ratio of dietary n-3 relative to n-6 fatty acids has been shown to inhibit the developmen

34 Dietary n-6 fatty acids have been associated with UC in prospect

35 turated fatty acids and in decreases in some n-6 fatty acids in normal and prcd-affected dogs.

36 3 fatty acid intake and its interaction with n-6 fatty acids in relation to the plasma inflammatory m

37 ts in an abundance of n-3 and a reduction in n-6 fatty acids in the organs and tissues of these mice,

38 We previously showed that dietary n-6 fatty acids increase cancer cell adhesion to extrace

39 ion between lipid concentrations and dietary n-6 fatty acid intake (in whites) and long-chain n-3 fat

40 Higher or lower n-6 fatty acid intake did not significantly modify the r

41 Significant genotype-by-n-6 fatty acid intake interactions were observed only in

42 ciations of total or individual n-3 or total n-6 fatty acid intake with LTL in US males.

43 cant associations between total n-3 or total n-6 fatty acid intakes and LTL.

44 content are causal, optimization of n-3 and n-6 fatty acid intakes could improve retention of cognit

45 d clinical studies have established that the n-6 fatty acid, linoleic acid (LA), and the n-3 fatty ac

46 (K(d) from 28 to 53 nm) over polyunsaturated n-6 fatty acids, linoleic acid, and arachidonic acid (K(

47 nts [ie, a diet with a relative reduction in n-6 fatty acid (LOW n-6) or a diet with a relative incre

48 diovascular disease; however, high intake of n-6 fatty acids may attenuate the known beneficial effec

49 Omega-3 (n-3) and omega-6 (n-6) fatty acids may contribute to oxidative stress and

50 cyclooxygenase and lipoxygenase products of n-6 fatty acid metabolism, and support is accumulating f

51 the effects of varying dietary ratios of n-3:n-6 fatty acids on cell signaling in a rat model of chem

52 tty acids and the ratio of long-chain n-3 to n-6 fatty acids (P < 0.055).

53 However, there are indications that the n-6 fatty acids perform functions in experimental prosta

54 fatty acids predominating and very good n-3/n-6 fatty acids ratio.

55 Using mean intakes of n-3 and n-6 fatty acids reported on two 24-hour dietary recalls,

56 ne, PC-3, delivery of exogenous n-3 (but not n-6) fatty acids resulted in up-regulation of syndecan 1

57 d our awareness of the importance of n-3 and n-6 fatty acids; shown that trans fatty acids inhibit de

58 The n-3 and n-6 fatty acids shunt eicosanoid production away from th

59 have shown that n-3 fatty acids inhibit and n-6 fatty acids stimulate prostate tumor growth, but whe

60 High intake of n-6 fatty acids, through their effects on inflammation a

61 s reduced 25%, while the proportion of total n-6 fatty acids was reduced in the major phospholipid cl

62 Dietary and adipose tissue n-6 fatty acids were highly correlated: 18:2 (r = 0.58)

63 cytokine levels and HBI, whereas the % total n-6 fatty acids were inversely correlated with pro-infla