As shown in Table 3, the average total body weight (and thus weight gain) after 110 days was the same of rats fed the two high fat (high energy) diets, whereas the rats fed on the lower energy reference diet had a lower weight gain, as expected.
Other biometrical data show that there are no notable differences between the groups. Rats in the two high fat dietary groups had the same daily feed intake and their water intake was also the same (data not shown). The reference group consumed somewhat more feed than rats in the two high fat groups, but their daily energy intake was lower, explaining their lower weight gain. In conclusion, the experiment showed that the oil composition of the present invention does not affect performance of rats fed a high fat diet and there were no signs of adverse effects on the animals.
When the animals were sacrificed after 110 days of feeding and the bellies opened up, a notable difference between the two high-fat groups could be observed with the naked eye: Rats on the experimental high-fat diet supplemented with the oil composition of the present invention, had visibly less visceral fat than the corresponding high-fat group, resembling more the visceral fat accumulation in rats that had been fed on the low fat reference diet, when comparing rats of about same size. Statistical analysis of the weights of visceral fat in the three groups confirmed this direct visual observation. Since the amount of visceral fat increases with body size, independent on feeding regime, the primary data on perirenal fat in the three dietary groups have been plotted as a function of body weight at sacrifice, as shown in Figure 1.
Statistical treatment of these weight data revealed the following: There was a clear linear correlation between visceral fat weight and body weight in all three groups, with a level of statistical significance of p = 0.034 for the reference group (Control), p = 0.003 for the high-fat group (HF) and p = 0.018 for the experimental group containing the oil composition of the present invention (HF + 1.5% CO). Based on the fact that a statistically significant correlation exists between visceral fat weight and body weight, the statistical difference between the groups could be calculated by ANCOVA analysis, using weight as a covariate. The analysis showed that the difference between the group containing the experimental oil and the corresponding high- fat diet was statistically significant (p = 0.00241), whereas there was no statistically significant difference between the experimental oil group and the low fat group. The experimental oil group and the low fat reference group, taken together, were significantly different from the high-fat group (p = 0.0084). In conclusion therefore, the oil of the present invention, given as a minor supplement to high fat obesity inducing diet, inhibits the accumulation of visceral fat.
Figure 2 shows the glucose oxidation capacity of heart muscle tissue of rats which had been feeding on the three diets. Rats on the high-fat diet (HF) had reduced glucose oxidation capacity compared to rats on the low-fat control diet (Control), whereas in rats that had been fed on the high-fat diet containing 1.5 % of the present oil composition (HF + 1.5% CO), glucose oxidation capacity was comparable to that of the low- fat control rats. It is evident therefore that the present oil composition may counteract deterioration of healthy heart function even after long time feeding on an obesity inducing high-fat diet.
Figure 3 (A) shows the blood glucose levels during intraperitoneal glucose tolerance test in mice given the control diet (Control), high fat diet (HF) and high fat diet with oil composition (HF + 1.5% CO), respectively. Figure 3 (B) shows the area under the glucose tolerance curves shown in panel A. Data are expressed as mean ± SE. *P < 0.05 for HF vs Control; #P < 0.05 for HF + 1.5% CO vs HF. Blood glucose levels were significantly increased during the intraperitoneal glucose tolerance test in the HF mice compared with the Control mice. These results show that feeding with a high fat diet for 50 days induced insulin resistance characteristic of type 2 diabetes. Importantly, inclusion of 1.5% of the oil composition of the present invention to the high fat diet counteracted the development of insulin resistance.
Mice on the high fat diet (HF) had reduced myocardial glucose oxidation rates compared to mice on the control diet (Control) (p < 0.05). Glucose oxidation was partly restored, however, in mice that had been fed the high fat diet containing 1.5 % of the present oil composition (HF + 1.5% CO) (p < 0.05). It is evident, therefore, that the oil composition of the present invention may counteract the reduction in myocardial glucose oxidation capacity which occur after feeding with a high fat diet.
As shown in Table 3, the average total body weight (and thus weight gain) after 110 days was the same of rats fed the two high fat (high energy) diets, whereas the rats fed on the lower energy reference diet had a lower weight gain, as expected.Other biometrical data show that there are no notable differences between the groups. Rats in the two high fat dietary groups had the same daily feed intake and their water intake was also the same (data not shown). The reference group consumed somewhat more feed than rats in the two high fat groups, but their daily energy intake was lower, explaining their lower weight gain. In conclusion, the experiment showed that the oil composition of the present invention does not affect performance of rats fed a high fat diet and there were no signs of adverse effects on the animals.When the animals were sacrificed after 110 days of feeding and the bellies opened up, a notable difference between the two high-fat groups could be observed with the naked eye: Rats on the experimental high-fat diet supplemented with the oil composition of the present invention, had visibly less visceral fat than the corresponding high-fat group, resembling more the visceral fat accumulation in rats that had been fed on the low fat reference diet, when comparing rats of about same size. Statistical analysis of the weights of visceral fat in the three groups confirmed this direct visual observation. Since the amount of visceral fat increases with body size, independent on feeding regime, the primary data on perirenal fat in the three dietary groups have been plotted as a function of body weight at sacrifice, as shown in Figure 1.Statistical treatment of these weight data revealed the following: There was a clear linear correlation between visceral fat weight and body weight in all three groups, with a level of statistical significance of p = 0.034 for the reference group (Control), p = 0.003 for the high-fat group (HF) and p = 0.018 for the experimental group containing the oil composition of the present invention (HF + 1.5% CO). Based on the fact that a statistically significant correlation exists between visceral fat weight and body weight, the statistical difference between the groups could be calculated by ANCOVA analysis, using weight as a covariate. The analysis showed that the difference between the group containing the experimental oil and the corresponding high- fat diet was statistically significant (p = 0.00241), whereas there was no statistically significant difference between the experimental oil group and the low fat group. The experimental oil group and the low fat reference group, taken together, were significantly different from the high-fat group (p = 0.0084). In conclusion therefore, the oil of the present invention, given as a minor supplement to high fat obesity inducing diet, inhibits the accumulation of visceral fat.Figure 2 shows the glucose oxidation capacity of heart muscle tissue of rats which had been feeding on the three diets. Rats on the high-fat diet (HF) had reduced glucose oxidation capacity compared to rats on the low-fat control diet (Control), whereas in rats that had been fed on the high-fat diet containing 1.5 % of the present oil composition (HF + 1.5% CO), glucose oxidation capacity was comparable to that of the low- fat control rats. It is evident therefore that the present oil composition may counteract deterioration of healthy heart function even after long time feeding on an obesity inducing high-fat diet.Figure 3 (A) shows the blood glucose levels during intraperitoneal glucose tolerance test in mice given the control diet (Control), high fat diet (HF) and high fat diet with oil composition (HF + 1.5% CO), respectively. Figure 3 (B) shows the area under the glucose tolerance curves shown in panel A. Data are expressed as mean ± SE. *P < 0.05 for HF vs Control; #P < 0.05 for HF + 1.5% CO vs HF. Blood glucose levels were significantly increased during the intraperitoneal glucose tolerance test in the HF mice compared with the Control mice. These results show that feeding with a high fat diet for 50 days induced insulin resistance characteristic of type 2 diabetes. Importantly, inclusion of 1.5% of the oil composition of the present invention to the high fat diet counteracted the development of insulin resistance.Mice on the high fat diet (HF) had reduced myocardial glucose oxidation rates compared to mice on the control diet (Control) (p < 0.05). Glucose oxidation was partly restored, however, in mice that had been fed the high fat diet containing 1.5 % of the present oil composition (HF + 1.5% CO) (p < 0.05). It is evident, therefore, that the oil composition of the present invention may counteract the reduction in myocardial glucose oxidation capacity which occur after feeding with a high fat diet.
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