Fully hydrogenated canola oil extends lifespan in stroke-prone spontaneously hypertensive rats.

BACKGROUND: Canola oil (Can) and several vegetable oils shorten the lifespan of stroke-prone spontaneously hypertensive rats (SHRSP). Although similar lifespan shortening has been reported for partially hydrogenated Can, the efficacy of fully hydrogenated oils on the lifespan remains unknown. The present study aimed to investigate the lifespan of SHRSP fed diets containing 10 % (w/w) of fully hydrogenated Can (FHCO) or other oils. METHODS: Survival test: Upon weaning, male SHRSP were fed a basal diet for rodents mixed with one of the test oils -i.e., FHCO, Can, lard (Lrd), and palm oil (Plm) throughout the experiment. The animals could freely access the diet and drinking water (water containing 1 % NaCl), and their body weight, food intake, and lifespan were recorded. Biochemical analysis test: Male SHRSP were fed a test diet with either FHCO, Can, or soybean oil (Soy) under the same condition, except to emphasize effects of fat, that no NaCl loading was applied. Soy was used as a fat source in the basal diet and was set the control group. Blood pressures was checked every 2 weeks, and serum fat levels and histological analyses of the brain and kidney were examined after 7 or 12 weeks of feeding. RESULTS: During the survival study period, the food consumption of FHCO-fed rats significantly increased (15-20 % w/w) compared with that of rats fed any other oil. However, the body weight gain in the FHCO group was significantly less (10-12 %) than that in the control group at 9-11 weeks old. The FHCO (> 180 days) intervention had the greatest effect on lifespan, followed by the Lrd (115 ± 6 days), Plm (101 ± 2 days), and Can (94 ± 3 days) diets. FHCO remarkably decreased the serum cholesterol level compared with Can and the systolic blood pressure from 12 to 16 weeks of age. In addition, while some rats in the Can group exhibited brain hemorrhaging and renal dysfunction at 16 weeks old, no symptoms were observed in the FHCO group. CONCLUSION: This current study suggests that complete hydrogenation decreases the toxicity of Can and even prolongs the lifespan in SHRSP.

Testosterone-lowering activity of canola and hydrogenated soybean oil in the stroke-prone spontaneously hypertensive rat.

Canola and some other types of oil unusually shorten the survival of stroke-prone spontaneously hypertensive rats (SHRSP), compared with soybean oil, perilla oil and animal fats. Since differential effects of canola and soybean oil on steroid hormone metabolism were suggested by a preliminary DNA microarray analysis as a reason for this, the steroid hormone levels in the serum and tissues of SHRSP fed different oils were investigated. The testosterone levels in the serum and the testes were found to be significantly lower in the canola oil group than in the soybean oil group, while no significant differences were detected in the corticosterone and estradiol levels in tissues. In a second experiment, it was found that hydrogenated soybean oil, with a survival-shortening activity comparable to that of canola oil, also decreased the testosterone level in testes to a similar degree. The testosterone-lowering activity of canola and hydrogenated soybean oil observed in SHRSP was considered in relation to other factors possibly affecting the physiology of SHRSP.

Exploration for unknown substances in rapeseed oil that shorten survival time of stroke-prone spontaneously hypertensive rats. Effects of super critical gas extraction fractions.

To identify the causative substances for the shortening of survival time by rapeseed (Canola) oil in stroke-prone spontaneously hypertensive rats (SHRSP), SHRSP were fed on a standard chow supplemented with 10 w/w% soybean oil (control), rapeseed oil, one of the fractions of rapeseed oil obtained by super critical gas extraction (SCE) under a pressure of 180-bar or 350-bar, at 40 degrees C, or the residue from the extraction (with 0.5% NaCl in drinking water). In another series of experiment, SHRSP were fed for 8 weeks on the above-mentioned diets without salt loading and autopsied. Fatty acid compositions in these diets were similar, except in the soybean oil diet, and phytosterol contents were: (diet containing) 180-bar fraction>residue>rapeseed oil>350-bar fraction>soybean oil. Survival times in the rapeseed oil, 350-bar fraction and residue groups were shorter than, whereas that in the 180-bar fraction was similar to in the soybean oil group. In the 8-week feeding experiment, chronic nephropathy was found frequently in the groups other than the soybean oil group. The heart weights were higher in the rapeseed oil and residue groups. Cerebral necrosis was found in the residue group. Taken together, the followings are concluded, (1) Neither the fatty acid composition, nor the amount of phytosterols in the diets appeared to be decisive in the shortening of life. (2) SCE appeared to produce a safe (180-bar) fraction, though it failed to separate clearly the causative substances into specific fractions. (3) The factors that facilitate the genetic disease of SHRSP appear to exist in rapeseed oil. However, they might not be identical to those responsible for the life-shortening, since there were no findings common across the rapeseed oil, 350-bar and residue groups, which showed similar life-shortening.

Factors other than phytosterols in some vegetable oils affect the survival of SHRSP rats.

Unusual survival-shortening activities of some vegetable oils were detected in stroke-prone spontaneously hypertensive (SHRSP) rats, and phytosterol (PS) in the oils and the tissue tocopherol status have been suggested to be the factors for the activities. Here, we re-evaluated the contribution of PS to the survival-shortening, and examined the hepatic tocopherol status. A basal diet for rodents and a test oil were mixed at a 9:1 ratio, and the diet was given to male SHRSP rats upon weaning. The total and major PS contents of the diets and tissue lipids did not correlate with relative survival time. The free fatty acid fractions obtained by lipase and alkaline hydrolyses of canola oil (Can) and the original Can contained PS in comparable amounts but the free fatty acid fractions did not exhibit survival-shortening activities compared with the soybean oil (Soy) group. The activity was not detected in the ethyl acetate extracts of the aqueous phase after the hydrolysis. When a commercially available PS preparation was added to the Soy diet at an amount 2.8-fold higher than that in the Can diet, the mean survival time was shortened but was still significantly longer than that of the Can group. The hepatic tocopherol level was significantly higher in the Can group than in the hydrogenated Soy group and Soy group, but the former two groups exhibited a survival-shortening activity. These results indicate that factors other than PS, tocopherol status and fatty acid composition in some vegetable oils are critical for the survival-shortening activity observed in SHRSP rats.

Dietary canola and soybean oil fed to SHRSP rat dams differently affect the growth and survival of their male pups.

Canola oil (Can), as well as some other oils, shortens the survival of SHRSP rats compared with soybean oil (Soy). Although detrimental factors other than phytosterols have not been identified, they are likely to be hydrophobic and transmissible to pups. To test this possibility, female SHRSP rats (F0) were fed a diet supplemented with Can or Soy and mated at 11 wk of age. The growth of suckling pups (F1) from the Can-fed dams was significantly retarded compared with that of pups from the Soy-fed dams. Half of the male pups (F1) were weaned to the same diet as their dams (Can-->Can and Soy-->Soy groups) and the rest were weaned to the other diet (Can-->Soy and Soy-->Can groups). The survival rate of the male pups (F1) was significantly lower in the Can-->Can group than in the Soy-->Can group, and in the Can-->Soy group than in the Soy-->Soy group, indicating that the oils fed to dams differently affected the growth and survival of pups. There were fewer pups per dam in the Can-fed dams (F0) than in the Soy-fed dams, and in the dams (F1) of the Can-->Can and Soy-->Can groups than in those of the Can-->Soy and Soy-->Soy groups. Although Can is nutritionally detrimental to SHRSP rats compared with Soy, no direct evidence has been obtained thus far relating these observations to human nutrition.

Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the senescence- accelerated mouse.

Senescence-accelerated mouse-prone (SAMP1; SAMP1@Umz) is an animal model of senile amyloidosis with apolipoprotein A-II (apoA-II) amyloid fibril (AApoAII) deposits. This study was undertaken to investigate the effects of dietary fats on AApoAII deposits in SAMP1 mice when purified diets containing 4% fat as butter, safflower oil, or fish oil were fed to male mice for 26 weeks. The serum HDL cholesterol was significantly lower (P < 0.01) in mice on the diet containing fish oil (7.4 +/- 3.0 mg/dl) than in mice on the butter diet (38.7 +/- 12.5 mg/dl), which in turn had significantly lower (P < 0.01) HDL levels than mice on the safflower oil diet (51.9 +/- 5.6 mg/dl). ApoA-II was also significantly lower (P < 0.01) in mice on the fish oil diet (7.6 +/- 2.7 mg/dl) than on the butter (26.9 +/- 7.3 mg/dl) or safflower oil (21.6 +/- 3.7 mg/dl) diets. The mice fed fish oil had a significantly greater ratio (P < 0.01) of apoA-I to apoA-II, and a smaller HDL particle size than those fed butter and safflower oil. Severe AApoAII deposits in the spleen, heart, skin, liver, and stomach were shown in the fish oil group compared with those in the butter and safflower oil groups (fish oil > butter > safflower oil group, P < 0.05). These findings suggest that dietary fats differ in their effects on serum lipoprotein metabolism, and that dietary lipids may modulate amyloid deposition in SAMP1 mice.