• Journal of Nutrition and Health
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• v.29 no.6
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• pp.642-650
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• 1996

Apo E polymorphism (e2, e3, e4) was among the first reported genetic polymorphism that explained part of the normal variation in plasma cholesterol concentrations. Both alleles E2 and E4 are significantly more frequent in patients with mixed forms of hyperlipidemia and contribute on the observed differences in CHD risk among different populations. Effects of apo E polymorphism on the distribution of plasma lipid profiles were studied in 105 normolipidemic healthy women. The relative frequencies of common alleles for gene locus of apo E in this study were that E3 allele was 0.848, E4 allels was 0.087, and E2 allele was 0.067. SBP and DBP were slightly more elevated in E2 allele than those in E3 and E4. The pulsation was also significantly (p<0.016) increased by E2 allele with excess body fat % in E2 allele. There were no differences in total-, total HDL-, VLDL+LDL-, VLDL- and LDL cholesterol among the apo E alleles. However, apo E2 allele subject had lower level of total HDL and HDL2 cholesterol (P<0.047) and significantly higher lev디 of HDL3 cholesterol (P<0.05) than those in apo E3 and E4 allele subject. The conclusion is that first, it seems that apo E4-mediated alteration through LDL B/E receptors or E receptors in cholesterol metabolism results in lower plasma TG or remanate particles and in higher levels of VLDL+LDL or LDL. Second, apo E2 allele shows reciprocal effects of E4 on the plasma lipid metabolism, respecitvely. Third, apo E2 allele was more atherogenic than apo E4 because the higher levels of HDL3/HDL2 ratio and atherogenic index[(TC-HDL)/HDL]were criticized.

• Journal of Nutrition and Health
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• v.50 no.3
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• pp.225-235
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• 2017

Purpose: This study aimed to investigate the potential of freeze-dried persimmon powder (Diospyros kaki Thumb.) to protect against dyslipidemia induced by a high-fat/cholesterol diet (HFD) in a rat model. Methods: Fifty Wistar rats were randomly divided into five groups: normal control (NC), high-fat/cholesterol control (HC), tannin in HFD (HT, 1% of diet), immature persimmon in HFD (HI, 7% of diet), and mature persimmon in HFD (HM, 7% of diet). Tannin was used as a positive control. Biochemical, molecular, and histopathological changes were observed in the blood and liver. Results: We confirmed that a high fat/cholesterol diet successfully induced dyslipidemia, which was characterized by significantly altered lipid profiles in the plasma and liver. However, oxidized low-density lipoprotein levels, histopathological damage in the liver, and hepatic triglyceride levels were significantly reduced in all HT, HI, and HM groups compared to those in the HF group. In contrast, plasma apolipoprotein B level was significantly reduced only in the HT and HM groups, whereas reduction of the LDL-C level was detected only in the HI group. Although HF-induced sterol regulatory element-binding protein (SREBP) gene expression was significantly reduced in all treated groups, downstream gene expression levels varied among the different groups; significant reduction of fatty acid synthase (FAS) and 3-hydroxy-3-methylglutaryl-CoA (HMGCR) gene expression was detected only in the HI group, whereas cholesterol $7{\alpha}$-hydroxylase (CYP7A1) gene expression was significantly elevated only in the HM group. Conclusion: Taken together, the data suggest that protection of LDL oxidation and hepatic lipogenesis might be, at least partly, attributed to tannin in persimmons. However, the identified mechanisms varied up to the maturation stage of persimmon. In the case of immature persimmon, modulation of FAS and HMGCR gene expression was prominent, whereas in the case of mature persimmon, modulation of CYP7A1 gene expression was prominent.