In our previous paper, we reported that long-term feeding of high-fat and-cholesterol diet (HFC diet) suppressed the development of severe hypertension and reduced the incidence of stroke in stroke-prone spontaneously hypertensive rats (SHRSP). Very little is known, however, about the role of lipo-and apoproteins in relation to the reduction of strokes in SHRSP, although it is evident that long-term feeding of the HFC diet drastically changes the distribution of lipo-and apoproteins. Thus, it is useful for elucidation of the mechanism to investigate the changes in lipo-and apoproteins induced by long-term feeding of the HFC diet. In this paper, we examined the changes of lipo-and apoproteins by long-term (6 months) feeding of HFC diet to SHRSP (HFC-SHRSP) and Kyo: Wistar rats (HFC-WKY). SHRSP (C-SHRSP) and WKY (C-WKY) fed normal diets were used as controls.
The concentrations of total cholesterol (TC), triglyceride (TG) and high density lipoprotein (HDL)-cholesterol in C-SHRSP increased with age during the experimental period, while those of C-WKY were almost constant. Heparin-Sepharose affinity chromatography suggested that the increase of HDL-cholesterol in C-SHRSP was probably due to an age-related increase of HDL rich in apo A-I (apo A-I HDL).
In HFC-WKY, a decrease of HDL accompanied by a rapid increase of serum TC were observed after about 1 month on the HFC diet, then HDL increased to the same level or higher with prolonged feeding of the HFC diet in comparison with that of C-WKY. The increase of HDL seemed to be due to the increase of HDL rich in apo E (apo E HDL) including HDL
c. β-lipoprotein also increased gradually with prolonged feeding.
In HFC-SHRSP, the development of severe hypertension was partially suppressed and the incidence of stroke was reduced in comparison with C-SHRSP as reported previously. But, there was no increase of HDL as was seen in HFC-WKY, which was associated with the low content of both apo E HDL and apo A-I HDL. Moreover, the production of HDL
c was much less than that in HFC-WKY. On the other hand, there was a remarkable increase of β-lipoprotein associated with a large increase of apo B.
These changes suggest that different pathways of lipoprotein metabolism (presumably β-pathway of VLDL) might be accelerated and maintained by hypertension in HFC-SHRSP. Therefore, it seems to be reasonable that this accelerated atherogenic condition, contrary to our expectation, would attenuate severe hypertension and protect cerebral arteries from necrosis, which may result in the reduction of strokes.
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