It is generally accepted that a high-protein diet prevents the development of cerebrovascular lesions and improves the survival rate in studies using stroke-prone spontaneously hypertensive rats (SHRSP). Moreover, it is well documented that the preventive effect is largely due to attenuation of the development of severe hypertension. However, in addition to the reduction of blood pressure, there must be some other mechanisms which are nutritionally effective.
In order to elucidate nutritionally effective mechanisms, we investigated the prophylactic effect of a protein diet (the K diet) on the development of cerebrovascular lesions in SHRSP. The diet was composed of dried bonito protein as the protein source and contained the same amounts of protein as the control diet (the Funabashi SP diet). Experimental groups were maintained on the K diet from 5 (ca. 130mmHg), 8 (ca. 200mmHg) or 10 (ca. 230mmHg) weeks of age and the control group was maintained on the Funabashi SP diet, with free access to the diet and to drinking water.
In the experimental groups administered the K diet from 5 or 8 weeks of age, the development of hypertension was attenuated, there was a reduction of the incidence of cerebrovascular lesions and elongation of the life-span was observed. On the other hand, in the experimental group administered the K diet from 10 weeks of age, a reduction of the incidence of cerebrovascular lesions and an elongation of the life-span were observed without the reduction of blood pressure. Taking the above results into account, we investigated the serum lipid metabolism, which might be affected by the administration of the K diet.
The results obtained were as folows:
1. Serum levels of total cholesterol and high density lipoprotein (HDL) cholesterol in all experimental groups were not significantly different from those in the control group. However, among various serum apolipoproteins, only serum apoE content in every experimental group was significantly lower than that in the cotrol group.
2. The reduction in serum apoE content in every experimental group was due to a decrease in apoE content in the HDL fraction (d: 1.063-1.210), but there was no significant difference among the three experimental groups.
3. Subfractionation of the HDL fraction by Heparin-Sepharose 4B affinity chromatography revealed that HDL rich in apoE (apoE HDL) in every experimental group was markedly diminished in comparison with the control group, while HDL rich in apoA-I (apoA-I HDL) remained unchanged in all groups.
4. In conclusion, the reduction of apoE HDL was induced by the K diet feeding in every experimental group, and it was independent of the feeding stage. However, further studies using various kinds of food will be necessary to confirm a definite relationship between the reduction of apoE HDL and the prophylactic effect of the K diet.
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