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1 ns-11 and 38.5% trans-10,cis-12) or 4 g/d of safflower oil.
2 th safflower oil, or treated with DMH-11C in safflower oil.
3 thyl ester of either fish oil, olive oil, or safflower oil.
4        Maximum increases occurred 10 h after safflower oil; 14 h after cocoa utter, coconut oil, cano
5  were pair-fed on diets consisting of 1) 59% safflower oil, 2) 59% menhaden fish oil, or 3) 59% carbo
6 A; n-9 and n-3 rich), 3) a blend of corn and safflower oil (25:75) (CornSaff; n-6 rich), 4) a blend o
7 H versus TCA cycle flux was decreased in the safflower oil (43 +/- 8%) versus the control (73 +/- 8%,
8 (CornSaff; n-6 rich), 4) a blend of flax and safflower oils (60:40) (FlaxSaff; n-6 and short-chain n-
9 n was used to study the effects of palm oil, safflower oil, a mixture of fish and safflower oil, and
10  were consistent with complete absorption of safflower oil and the nonabsorbability of olestra and ca
11 ed by measuring absorption of well-absorbed (safflower oil) and poorly absorbed (olestra; calcium soa
12 lm oil, safflower oil, a mixture of fish and safflower oil, and olive oil on postprandial apolipoprot
13  a different fat: menhaden oil, herring oil, safflower oil, canola oil, coconut oil, or cocoa butter.
14 sumption of triacylglycerol-esterified LA in safflower oil did not increase plasma concentrations of
15                        In both genotypes the safflower oil diet blunted insulin-mediated suppression
16 s when the fish oil diet was replaced by the safflower oil diet.
17 loid precursor protein transgenic mice fed a safflower oil-enriched ("Bad") diet used to accelerate p
18                                         Pure safflower oil exhibited the highest total TPUFA (76.78%)
19 (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial
20  resistance (HGP, P = NS vs. PPAR-alpha null safflower oil-fed mice).
21  mice fed the fish oil diet as compared with safflower oil-fed mice.
22                                          The safflower oil-fed rats were insulin resistant compared w
23 in-stimulated glucose disposal attributed to safflower oil feeding was a consequence of reduced glyco
24 19, and 125 +/- 14 nmol x g(-1) x min(-1) in safflower oil, fish oil, and control, respectively) was
25 iglyceride (TG) content was increased in the safflower oil group (7.3 +/- 0.8 micromol/g) compared wi
26 n insulin-stimulated glucose disposal in the safflower oil group was associated with a lower rate of
27            After ingestion of a 50-g load of safflower oil in capsules (to preclude oral exposure to
28 s and detecting small quantities of corn and safflower oils in olive oil.
29 modified by incorporating varying amounts of safflower oil into the diet.
30 ic acid from herring oil, linoleic acid from safflower oil, linolenic acid from canola oil, lauric ac
31 trol diet or isocaloric diets containing 27% safflower oil or 27, 13.5, and 8% menhaden fish oil.
32  were fed isocaloric diets containing either safflower oil or fish oil for 2 weeks before the start o
33     When rats were fed a diet containing 10% safflower oil or menhaden fish oil, the level of hepatic
34 igh-fat diets containing 27% fat from either safflower oil or safflower oil with an 8% fish oil repla
35 ocaloric diets modified to include corn oil, safflower oil, or DFO (doses ranging from 0.75% to 6.00%
36 d a 5% lipid diet containing lard, lard plus safflower oil, or lard plus linseed oil for 10 weeks.
37  Animals were either untreated, treated with safflower oil, or treated with DMH-11C in safflower oil.
38 on than after sunflower oil (P: = 0.003) and safflower oil (P: = 0.001) supplementation.
39 ion than after sunflower oil (P: = 0.01) and safflower-oil (P: = 0.0003) supplementation.
40 ially available tocotrienol supplements or a safflower oil placebo for 28 d.
41  PPAR-alpha null mice fed the fish oil diet, safflower oil plus fish oil, hepatic insulin resistance
42 tion period a salad dressing containing 21 g safflower oil providing 16 g LA/d was added to the subje
43 s demonstrated that high dietary corn oil or safflower oil rich in omega-6 fatty acids increased the
44 ary oils, conjugated linoleic acid (CLA) and safflower oil (SAF), on body weight and composition in o
45 eatment with 4 g/d of ethyl esters of either safflower oil (SAF; control), eicosapentaenoic acid (EPA
46 oils (no supplementation, JO, fish oil [FO], safflower oil [SO], and arachidonic acid [AA]) were fed
47 TBARS was higher than with sunflower-oil and safflower-oil supplementation.
48 s were significantly lower after addition of safflower oil to the diet.
49  work investigates the extraction process of safflower oil using pressurized ethanol, and compares th
50 ; control birds were exposed via diet to the safflower oil vehicle only (24 pairs).
51 .8 and 31.7 +/- 1.9 mg x kg(-1) x min(-1) in safflower oil versus control and fish oil groups, respec
52                    To examine the effects of safflower oil versus fish oil feeding on in vivo intramu
53 tion [HGP], P < 0.002 vs. wild-type mice fed safflower oil), whereas in contrast, in PPAR-alpha null
54 taining 27% fat from either safflower oil or safflower oil with an 8% fish oil replacement (fish oil

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