Canola Oil Supplementation Research Articles

Canola oil inhibits human breast cancer cell growth by regulating caspase‐3 and p53

Epidemiological studies indicate that consuming a high‐fat diet may be correlated with an increased risk of breast cancer in women. However, increasing evidence suggests that it is not the quantity of fat but the type of fat intake that influences breast cancer risk. It is also suggested that the protective effect of omega‐3 fatty acids on breast cancer risk depends on the level of omega‐6 fatty acids, with a recommended omega‐6 to omega‐3 fatty acids ratio at 2:1 or lower. Canola oil has one of the lowest levels of saturated fat (7%, about half the level present in corn oil, olive oil and soybean oil). It has a relatively high level of oleic acid (monounsaturated fatty acid, 62%) and omega‐3 fatty acids (alpha‐linolenic, 10%) compared to most vegetable oils. It is thought that the low saturated fat, high oleic acid, and relatively high omega‐3 fatty acids content in canola oil give it particularly healthful properties. To investigate the effects of canola oil on breast cancer cell growth and apoptosis, two estrogen receptor‐positive breast cancer cell lines, T47D and MCF‐7, as well as a normal mammary cell line, MCF‐10A, were cultured and cell proliferation, caspase‐3 and p53 activities were measured. Canola oil supplementation significantly inhibited the growth of both T47D and MCF‐7 cell lines, but not MCF10A cell line. Canola oil also significantly increased the expression of p53, a tumor suppressor gene involved in cancer cell death, as well as the activity of caspase‐3 enzyme, one of the crucial enzymes regulating apoptosis pathway. Dietary strategies for cancer prevention and therapy are low‐risk and cost‐effective. Therefore, these results could be useful in the development of improved nutritional strategies for breast cancer prevention and therapy to reduce breast cancer risk. Supported by USDA‐CSREES (#2007‐38624‐18602).

Consumption of a Novel Dietary Formula of Plant Sterol Esters of Canola Oil Fatty Acids, in a Canola Oil Matrix Containing 1,3-Diacylglycerol, Reduces Oxidative Stress in Atherosclerotic Apolipoprotein E-Deficient Mice

The antiatherogenic properties of a novel dietary formula (PS-CO) of plant sterol esters of fatty acids, produced by enzymatic interesterification of plant sterols with canola oil (CO), in a CO matrix containing 1,3-diacylglycerol, were evaluated in apolipoprotein E-deficient mice. PS-CO consumption strongly tended to lower total plasma cholesterol levels by 21%, compared to the placebo group. Blood triglycerides were reduced by 38% and 36% compared to CO and placebo-fed mice, respectively. Serum lipid peroxide levels were lowered following PS-CO administration by 62% and 63%, compared to CO and placebo administration, respectively. Unlike CO supplementation, PS-CO consumption preserved serum paraoxonase (PON1) activity. Mouse peritoneal macrophages from PS-CO-fed mice exhibited reduced cellular uptake of oxidized-LDL compared to those from placebo-fed mice and demonstrated a tendency toward a decreased capability to release superoxide anions. These findings indicate that PS-CO supplementation is beneficial in reducing serum lipid levels, and serum and macrophage oxidative stress, thus contributing to the reduction in atherogenic risk factors.

Effect of supplementing corn- or barley-based feedlot diets with canola oil on faecal shedding of Escherichia coli O157:H7 by steers

This study was conducted to evaluate the effect of supplementing barley- or corn-based diets with canola oil on faecal shedding of Escherichia coli O157:H7 by experimentally inoculated feedlot cattle. Four groups of yearling steers fed on barley- or corn-based feedlot diets containing 0% (BA; CO) or 6% canola oil (BA-O; CO-O) were inoculated with 10(10) CFU of a mixture of four nalidixic acid-resistant strains of E. coli O157:H7. The inoculated strains were tracked in oral (mouth swab) and environmental (water, water bowl interface, feed, faecal pat) samples by enrichment and immunomagnetic separation (IMS) for 12 weeks, and in rectally collected faecal samples for 23 weeks (enumeration by dilution plating for 12 weeks; detection by IMS for a further 11 weeks). Levels of E. coli O157:H7 shed in faecal samples over the course of the enumeration period were similar (P = 0.14) among treatments. Disappearance of the inoculated strains from faeces was more rapid (P = 0.009) with barley than with corn, but shedding levels at the end of the enumeration period were similar (P = 0.21) across grain types. Canola oil supplementation did not affect (P = 0.71) the rate of disappearance of E. coli O157:H7 from faeces. The numbers of steers culture positive for E. coli O157:H7 during the enumeration period were similar (P = 0.57) among treatments. During the 11-week detection period, however, more (P < 0.001) steers were E. coli O157:H7-positive in the BA group (15/64) than in BA-O (two of 64), CO (two of 56), or CO-O (one of 56). The organism was present in two of 48 water samples (both CO-O), one of 48 water bowl swabs (BA-O), four of 48 feed samples (two of 12 BA; two of 12 CO-O), 30 of 48 pen floor faecal pat samples, and 296 of 540 mouth swabs (81/144 BA, 80/144 BA-O, 74/126 CO and 61/126 CO-O). Supplementing corn or barley-based diets with canola oil did not affect shedding of E. coli O157:H7 by feedlot cattle. High-shedding individuals (i.e. 'super shedders') may be responsible for disseminating E. coli O157:H7 among penmates. Faeces on pen floors appears to be a more significant source of infection than are feed or drinking water.

Effects of feeding or abomasal infusion of canola oil in Holstein cows. 1. Nutrient digestion and milk composition.

We determined the effects of feeding canola oil or infusing it into the abomasum on rumen fermentation, nutrient digestibility, duodenal flows of fatty acids, and milk composition in Holstein cows. Five ruminally and duodenally cannulated Holstein cows in late lactation were used in a 3 x 5 incomplete Latin square design. Treatments were 1) CONTROL: basal diet (CON), 2) CONTROL+supplementation of canola oil at 1 kg/d in the feed (FED), and 3) CONTROL+abomasal infusion of canola oil at 1 kg/d (INF). Compared with CON, feed intake, ruminal fermentation characteristics, ruminal and total tract digestibilities of nutrients were not significantly affected by FED treatment but duodenal flows and milk concentrations of fatty acids (FA) such as trans-11 18:1 and cis-9 trans-11 18:2 (conjugated linoleic acid, CLA) were increased. In contrast to the effects of FED, INF reduced feed intake, total VFA production, intestinal flows of nutrients, FA digestibility and yields of milk and milk fat. Both FED and INF significantly reduced the proportions of saturated and medium-chain FA, and increased cis 18:1 in milk. Concentrations of 18:2n-6 and 18:3n-3 in milk were increased nearly 2-fold with INF relative to CON. Dietary or postruminal supplementation of canola oil to late-lactation cows reduced saturated FA and increased unsaturated C18 in milk but nutrient digestion was adversely affected with abomasal infusion of canola oil.

Effects of feeding or abomasal infusion of canola oil in Holstein cows. 2. Gene expression and plasma concentrations of cholecystokinin and leptin

We determined the relative importance of cholecystokinin (CCK), leptin, and fatty acid concentrations in plasma in mediating the satiety effects of supplemental fat in lactating cows. Five ruminally and duodenally cannulated Holstein cows in late lactation were used in a 3 x 5 incomplete Latin square design with three treatments: 1) CONTROL: basal diet (CON), 2) CONTROL+supplementation of canola oil at 1 kg/d in the feed (FED) and 3) CONTROL+abomasal infusion of canola oil at 1 kg/d (INF). Relative to CON, feed intake was reduced by INF but not by FED. We provide evidence that both FED and INF treatments stimulated CCK gene expression in the duodenum and elevated plasma CCK concentrations. However, our results did not support a role for CCK in mediating satiety through an endocrine mechanism of action. We speculate that CCK might be acting either through paracrine and/or neurocrine routes to influence feed intake in cattle. Both FED and INF had no effect on the mRNA abundance of leptin, lipoprotein lipase, or acetyl-CoA carboxylase in adipose tissue. Plasma concentrations of leptin, insulin and IGF-I were not altered by FED or INF, indicating that these signals may not be involved in mediating short-term hypophagic effects of dietary fat. Plasma concentrations of 18:1n-9 and 18:2n-6 were significantly greater for INF than for FED or CON. We conclude that the hypophagic effects of supplemental fat in cattle depend on the amount of unsaturated fatty acids reaching the intestine and that this satiety effect is mediated through CCK, oleic acid and (or) linoleic acid, but leptin is not involved.

Effects of supplemental vitamin E and canola oil on tissue tocopherol and liver fatty acid profile of finishing swine.

We conducted a 4 x 3 factorial experiment with finishing pigs for 6 wk to evaluate effects of dietary canola oil and vitamin E on vitamin E status and liver fatty acid profile. Treatments consisted of four supplemental levels of vitamin E (0, 50, 125, and 200 mg/kg) and three of canola oil (0, 5, and 10% of the diet). Serum was collected each week and tissue samples at d 42. Dietary canola oil (P = .02) and vitamin E (P < .001) increased serum alpha-tocopherol. Serum alpha-tocopherol reached a plateau at d 35 of vitamin E and canola oil supplementation. An interaction was observed between canola oil and vitamin E (P = .02) for liver alpha-tocopherol. Liver alpha-tocopherol was greater in pigs fed diets with 10% canola oil and supplemented with 125 or 200 mg/kg of vitamin E than in pigs fed diets with 0 and 5% canola oil. An interaction also occurred between canola oil and vitamin E (P = .01) for alpha-tocopherol in the gluteus medius and obliquus capitis caudalis muscles. A greater magnitude of increase in muscle alpha-tocopherol was observed in pigs fed diets with no canola oil than in pigs fed diets with 5 and 10% canola oil. Highest alpha-tocopherol was in liver, followed by obliquus capitis caudalis and then gluteus medius. Inclusion of 5 or 10% dietary canola oil decreased the amount of saturated fatty acids by 4.1 and 13.5%, increased monounsaturated fatty acids by 10.9 and 39.3%, respectively, and had no effect (P > .10) on total polyunsaturated fatty acids. Canola oil increased linoleic acid [18:2(n-6)] (quadratic, P = .05) and linolenic acid [18:3(n-3)] (linear, P < .001) while decreasing arachidonic acid [20:4(n-6)] and docosadienoic acid (20:2) linearly (P < .001 and P = .02, respectively). Dietary canola oil and vitamin E increased serum and tissue alpha-tocopherol; canola oil increased monounsaturated and decreased saturated fatty acids in liver.

Effect of dietary canola and reference oils upon serum lipids and platelet aggregation

To compare Canola a terrestrial (n-3) oil with fish oil (n-3) and common vegetable oil (n-6) in decreasing serum lipids and platelet aggregation, various oils were included in Chow ®-based diets and fed to rats in an eight-weeks feeding trial. The Chow ® diet contained 2% cholesterol along with either Canola, menhaden, safflower, or partially hydrogenated soy oil, or no oil addendum. The menhaden oil group was the only one to show a significant reduction in serum cholesterol and triglycerides and at the same time yielded the most uniform decrease in platelet aggregability. However, this same group was also the only one to show a decrease in serum tocopherol levels, suggesting that improving an atherogenic risk profile may require antioxidant supplementation. In these rat trials, Canola oil supplementation did not yield the same results measured during menhaden supplementation.