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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.
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
17 loid precursor protein transgenic mice fed a safflower oil-enriched ("Bad") diet used to accelerate p
19 (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial
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
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.
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
49 work investigates the extraction process of safflower oil using pressurized ethanol, and compares th
51 .8 and 31.7 +/- 1.9 mg x kg(-1) x min(-1) in safflower oil versus control and fish oil groups, respec
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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