Hypercholesterolemic

Vanhanen, H. X, Blomqvist, S., Ehnholm, C., et al., 1993. Sernm cholesterol, cholesterol precursors, and plant sterols in hypercholesterolemic subjects widi different apoE phenotypes during dietary sitostanol ester treatment. Journal of Lipid Research 34 1535-1544. 

GARDNER c D, NEWELL K A, CHERiN R and HASKELL w L (2001) The effect of soy protein with or without isoflavones relative to milk protein on plasma lipids in hypercholesterolemic postmenopausal women. dm J Clin Nutr. 73 (4) 728-35. 

SIRTOR] C R, BOSISIO R, PAZZUCCONI F, BONDIOLI A, GATTI E, LOVATI M R and MURPHY P (2002) Soy Milk with a High Glycitein Content Does Not Reduce Low-Density Lipoprotein Cholesterolemia in Type II Hypercholesterolemic Patients. Nutr Metab. 46 (2) 88-92. 

WANGEN K E, DUNCAN A M, XU x and KURZER M s (2001) Soy isoflavones improve plasma lipids in normocholesterolemic and mildly hypercholesterolemic postmenopausal women. Am J Clin Nutr. 73 (2) 225-31. 

In our study, consumption of rye bread or rye bread with phloem did not have an effect on serum lipids (total, LDL or HDL cholesterol or triglycerides) (Table 14.4). This is contrary to a recent finding suggesting that soluble fiber from rye bread decreased the concentrations of cholesterol (Leinonen et al., 2000). In that study ingestion of rye bread (220 g/d) with naturally high amounts of insoluble (18 g/d) and soluble fiber (4 g/d) decreased the LDL concentrations by 8% in hypercholesterolemic men. The researchers speculated that soluble fiber, maybe P-glucan, was responsible for the hypocholesterolemic effect. The amount of rye bread (70 g/d vs 220 g/d), the amount of total (5.9-11.8 g/d vs 22.1 g/d) and soluble fiber (0.6-1.3 g/d vs 4 g/d) ingested in this study was considerably less, and could explain the lack of effects on blood lipids in our study. 

LICHTENSTEIN A H, AUSMAN L M, CARRASCO W, GUALLEIRI L J, JENNER J L, ORDOVAS J M, NICOLOSI R J, GOLDIN B R, SCHAEFER E J (1994) Rice bran oil consumption and plasma lipid levels in moderately hypercholesterolemic humans. Arterioscleroses and Thrombosis, 14(4) 549-556. 

QURESHI A A, BRADLOw B A, SALSER w A, BRACE L D (1997) Novel tocotiienols of rice bran modulate cardiovascular risk parameters of hypercholesterolemic humans. J Nutri Biochem, 8 290-8. 

QURESHI A A, SAMI s A, SALSER w A, KHAN F A (2001) Syuergistic effect of tocotrienol rich fraction (TRF 25) of rice bran and lovostatin on lipid parameters in hypercholesterolemic hamnns. J Nutri Biochem, 12 318-29. 

WESTSTRATE J A, MEIJER G w (1998) Plant sterol emiched margarine and reduction of plasma and total LDL-cholesterol concentrations in normocholesterolemic and mildly hypercholesterolemic sahjects.. Eur J Clin Nutr, 52(5) 334-43. 

Caligiuri G, Levy B, Pemow J, Thoren P, Hansson GK. Myocardial infarction mediated by endothelin receptor signaling in hypercholesterolemic mice. Proc Natl Acad Sci U S A 1999 96(12) 6920-6924. 

Yu X, Dluz S, Graves DT, et al. Elevated expression of monocyte chemoattractant protein 1 by vascular smooth muscle cells in hypercholesterolemic primates. Proc Natl Acad Sci U S A 1992 89(15) 6953-6957. 

Rezaie-Majd A, Maca T, Bucek RA, et al. Simvastatin reduces expression of cytokines interleukin-6, interleukin-8, and monocyte chemoattractant protein-1 in circulating monocytes from hypercholesterolemic patients. Arterioscler Thromb Vase Biol 2002 22(7) 1194-1199. 

CCR2 deficiency results in decreased atherosclerosis in vessels of susceptible mice. 2. Decreased intimal hyperplasia in femoral artery injury model of atherosclerosis seen with CCR2 deficiency. CCR2 expression is increased in the monocytes of hypercholesterolemic patients. 

Carranza MJ, Herrera AJ, Alvizouri MM, Alvarado JM and Chavez CF. 1997. Effects of a vegetarian diet vs a vegetarian diet enriched with avocado in hypercholesterolemic patients. Arch Med Res 28(4) 537-541. 

Fernandez LM, Lin ECK, Trejo A and McNamara DJ. 1992. Prickly pear (Opuntia sp.) pectin reverses low density lipoprotein receptor suppression induced by a hypercholesterolemic diet in Guinea Pigs. J Nutt 122 2330-2340. 

Wang-Polagruto JF, Villablanca AC, Polagruto JA, Lee L, Holt RR, Schrader HR, Ensunsa JL, Steinberg FM, Schmitz HH and Keen CL. 2006. Chronic consumption of flavanol-rich cocoa improves endothelial function and decreases vascular cell adhesion molecule in hypercholesterolemic postmenopausal women. J Cardiovasc Pharmacol 47 Suppl 2 S177-186 discussion S206-209. 

Martin-Carron N, Goni I, Larrauri JA, Garcia-Alonso A and Saura-Calixto F. 1999. Reduction in serum total and LDL cholesterol concentrations by a dietary fiber and polyphenol-rich grape products in hypercholesterolemic rats. Nutr Res 19 1371-1381. 

Hallikainen MA, Sarkkinen ES and Uusitupa MIL 2000. Plant stanol esters affect serum cholesterol concentrations of hypercholesterolemic men and women in a dose-dependent manner. J Nutr 130 767-776. 

High antioxidative activity carvedilol has been shown in isolated rat heart mitochondria [297] and in the protection against myocardial injury in postischemic rat hearts [281]. Carvedilol also preserved tissue GSL content and diminished peroxynitrite-induced tissue injury in hypercholesterolemic rabbits [298]. Habon et al. [299] showed that carvedilol significantly decreased the ischemia-reperfusion-stimulated free radical formation and lipid peroxidation in rat hearts. Very small I50 values have been obtained for the metabolite of carvedilol SB 211475 in the iron-ascorbate-initiated lipid peroxidation of brain homogenate (0.28 pmol D1), mouse macrophage-stimulated LDL oxidation (0.043 pmol I 1), the hydroxyl-initiated lipid peroxidation of bovine pulmonary artery endothelial cells (0.15 pmol U1), the cell damage measured by LDL release (0.16 pmol l-1), and the promotion of cell survival (0.13 pmol l-1) [300]. SB 211475 also inhibited superoxide production by PMA-stimulated human neutrophils. 

A comprehensive, randomized, placebo-controlled trial of infused bolus L-arg and its enantiomer (D-arg) included healthy subjects, non-insulin dependent diabetics, hypertensive subjects, and normotensives with primary hypercholesterolemia [147]. A blood-pressure drop and an acute inhibition of ADP-induced aggregation in platelet-rich plasma were observed in all subjects after L-arg administration (<5 g). Both responses to L-arg infusion closely correlated in magnitude, were weaker in noninsulin dependent diabetics and hypercholesterolemics, and declined with increasing age. Notably, D-arg did not elicit any of the L-arg effects, which were reduced by some 70% when superimposed upon ongoing, nonselective NOS inhibition with infused L-N-monomethyl-arginine (L-NMMA). Since D-arg is not a NOS substrate, and L-NMMA is a substrate-competitive NOS inhibitor, the L-arg effects observed in this study were theorized to reflect a rise in vascular NO production by eNOS. In contrast, the inhibition of platelet aggregation observed in vitro after a 5 min L-arg infusion (160 mg total dose) into healthy subjects and patients with angiographic... 

G16. Ghiselli, G., Gaddi, A., Barozzi, G., Ciarrocchi, A., and Descovich, G., Plasma lipopro-tein(a) concentration in familial hypercholesterolemic patients without coronary artery disease. Metab., Clin. Exp. 41, 833-838 (1992). 

L15. Leren, T. P., Hjermann, I., Foss, O. P., Leren, P., and Berg, K., Long term effect of lovastatin alone and in combination with cholestyramine on lipoprotein(a) levels in familial hypercholesterolemic subjects. Clin. Invest. 70, 711-718 (1992). 

L. Anila and N.R. Vijayalakshmi, Antioxidant action of flavonoids from Mangifera indica and Emblicas officinalis in hypercholesterolemic rats. Food Chem. 83 (2003) 569-574. 

Kang, S. Y., Kim, S. H., Schini-Kerth, V. B., and Kim, N. D. (1995a). Dietary ginsenosides improve endothelium-dependent relaxation in the thoratic aorta of hypercholesterolemic rabbit. Gen. Pharmacol. 26, 483—487. 

Figure 4 Hypercholesterolemic rabbit carotid artery 30 days after balloon injury. Photomicrographs of Verhoff s tissue elastin staining of (A,C) full-size and (B,D) higher magnification sections from (A,B) control, (C,D) liposomal alendronate treated (3mg/kg intravenous, at the time of injury). Control animals were treated with buffer, free BP (alendronate), or empty liposomes and grouped as control (n — 20 arteries/group, P<0.05). Abbreviation BP, bisphosphonate.

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