Effects of dietary hypercholesterolemia on plasma lipids levels male and female Japanese white and heterozygous Kurosawa-Kusanagi hypercholesterolemic rabbits
DOI:
https://doi.org/10.24297/jab.v4i2.5573Keywords:
heterozygous hypercholesterolemic rabbits, cholesterol feeding, plasma cholesterol level, hypercholesterolemia.Abstract
High plasma cholesterol levels constitute a major risk factor for coronary heart diseases. In this study, we compared the response to dietary hypercholesterolemia with respect to plasma lipids levels in male and female Kurosawa-Kusanagi hypercholesterolemic (KHC) rabbits, which have Low density lipoprotein (LDL) receptor deficiency. Male and female Japanese white (JW) and heterozygous KHC rabbits were given a standard milled rabbit diet or diets with different concentrations of cholesterol. All the male and female JW and KHC rabbits given a standard milled rabbit diet did not show increased plasma cholesterol levels over the 24-week experiments. The plasma cholesterol levels in male JW rabbits fed a 0.1 % cholesterol-containing diet did not increase, but the levels in male heterozygous KHC rabbits fed the same diet transiently increased for 4-8 weeks (to 300 mg/dL) and then gradually decreased till the initial level. In contrast, in female JW rabbits fed the same diet, the plasma cholesterol  levels increased for 4-24 weeks (to 300 mg/dL), and in heterozygous KHC rabbits, the levels gradually increased (to 675 mg/dL after 24 weeks) after consumption of the 0.1 % cholesterol-containing diet. In ovariectomized JW and KHC rabbits fed the 0.1 % cholesterol-containing diet, the plasma cholesterol levels were half value the levels in non-ovariectomized rabbits  after 24 weeks. Gene expression of the LDL receptor in the liver significantly increased in male JW and KHC rabbits, but significantly decreased in female KHC rabbits. These results indicate that female rabbits had a greater response to the cholesterol diet than male rabbits and that the responsiveness to dietary hypercholesterolemia was predominantly genetic.Downloads
Download data is not yet available.
References
[1] Multiple risk factor intervention trial research groups. Multiple risk factor intervention trial. Risk factor changes and mortality results. JAMA 1989; 248: 1465-1477. [2] Denke MA. Review of human studies evaluating individual dietary Responsiveness in patients with hypercholesterolemia. Am J Clin Nutr 1995; 62: 471S-477. [3] Goldstain JL, Hobbs H, Brown MS. Familial hypercholesterolemia. In The metabolic and molecular bases of inherited disease. Ed 8. Edited by Scriver C, Beaudet A, Sly W, Valle D. New York: McGraw-Hill. 2001, p2863-2913 [4] Mabuchi H, Nohara A, Noguchi T, Kobayashi J, Kawashiri MA, Tada H, Nakanishi C, Mori M, Yamagishi M, Inazu A, Koizumi J. Molecular genetic epidemiology of homozygous familial hypercholesterolemia in the Hokuriku distinct of Japan. Atherosclerosis 2011; 214: 404-7. [5] Mabuchi H, Miyamoto S, Ueda K, Oota M, Takegoshi T, Wakasugi T, Takeda R. Caises of death in patients with familial hypercholesterolemia. Atherosclerosis 1986; 61: 1-6. [6] Stone HJ, Levy RI, Fredrickson DS, Verter J. Coronary artery disease in 116 kindred with familial type II hyperlipoproteinemia. Circulation 1974; 49: 476-488. [7] McGill HC, Stern MP. Sex and atherosclerosis. Atheroscler Rev 1979; 4:157-242. [8] Robinson RW, Hijano N, Cohen DB. Increased incidence of coronary heart disease in women castrated prior to the menopause. Arch Intern Med 1959; 104: 908-913. [9] Parrish HM, Carr CA, Hall DG, King TM. Time interval from castration in premenopausal women to development of excessive coronary atherosclerosis. Am J Obstet Gyneco 1967; 99: 155-162. [10] Barrett-Conner E, Bush TL. Estrogen and coronary heart disease in women. JAMA 1991; 265: 1861-7. [11] Stampfer MJ, Colditz GA. Estrogen replacement therapy and coronary heart disease: a quantitative assessment of the epidemiologic heart disease. Prev Med 1991; 20: 47-63. [12] Stampfer MJ, Colditz GA, Willett WC, Manson JE, Rosner B, Speizer FE, Hennekens CH. Postmenopausal estrogen therapy and cardiovascular disease. N Engl J Med 1991; 325: 756-762.
346 | P a g e M a r c h 0 7 , 2 0 1 4
[13] Rosamond W, Flegal K, Friday G, Furie K, Go A, Greenland K, Haase N, Ho M, Howard V, Kissela B, Kittner S, LloydJones D, McDermott M, Meigs J, Moy C, Nichol G, O’Donnell CJ, Roger V, Rumsfeid J, Sorlie P, Steinberger J,Thom T, Wasserthiel-Smoller S, Hong Y and for the merican Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2007; 115: e69-171. [14] Bronzert TJ, Brewer HB. New micromethod for measuring cholesterol in plasma lipoprotein fractions. Clin Chem 1977; 23: 2089-2098. [15] Folch BJ, Lees M, Sloanestanley GH. A simple method for the isolation and purification of total lipids from animal tissues. J Biol Chem 957; 226: 497-509. [16] Chirgwin JM, Przybyla AE, MacDonald RJ, RutterWJ. Isolation of biologically active ribonucleic acid from sources enriched in ribonuclease. Biochemistry 1979; 18: 5294–9. [17] Yamamoto T, Bishop RW, Brown MS, Goldstein JL, Russell DW. Deletion in cysteine-rich region of LDL receptor impedes transport to cell surface in WHHL rabbit. Science 1986; 232: 1230-7. [18] Kita T, Nagano Y, Yokode M, Ishii K, Kume N, Ooshima A, Yoshida H, Kawai C. Probucol prevents the progression of atherosclerosis in Watanabe heritable hyperlipidemic rabbit, an animal model for familial hypercholesterolemia. Proc Natl Acad Sci USA 1987; 84: 5928-5931. [19] Walsh BW, Schiff I, Rosner B, Greenberg L, Ravnikar V, Sacks F. Effects of postmenopausal estrogen replacement on the concentrations and metabolism of plasma lipoproteins. N Engl J Med 1991; 325: 1196–1204. [20] Ogita H, Node K, Kitakaze M. The role of estrogen and estrogen-related drugs in cardiovascular diseases. Curr Drug Metab 2003; 4: 497–504. [21] Wren BG. The effect of estrogen on the female cardiovascular system. Med J Aust 1992; 157: 204–8. [22] Chao Y, Windler EH, Chen GC, Havel RJ. Hepatic catabolism of rat and human lipoproteins in rats treated with 17alpha-ethinyl estradiol. J Biol Chem 1979; 254: 11360–6. [23] Roach PD, Noel S-P. Solubilisation of the 17-alpha ethinyl estradiol-stimulated low density lipoprotein receptor of male rat liver. J Lipid Res 1985; 26: 713–720. [24] Ma PTS, Yamamoto T, Goldstein JL, Brown MS. Increased mRNA for low density lipoprotein receptor in livers of rabbits treated with 17・-ethinyl estradiol. Proc Natl Acad Sci USA 1986; 83: 792–6. [25] Ferreri F, Naito NK. Effect of estrogens on rat serum cholesterol concentrations: Consideration of dose, type of estrogen and treatment duration. Endocrinol 1978; 102: 1621–7. [26] Owen AJ, Roach PD, Abbey M. Regulation of Low-Density Lipoprotein Receptor Activity by Estrogens and Phytoestrogens in a HepG2 Cell Model. Ann Nutr Metab 2004; 48: 269-275. [27] Ma P, Yamamoto T, Goldstein J, Brown MS. Increased mRNA for low density lipoprotein receptor in livers of rabbits treated with 17 alpha-ethinyl estradiol. Proc Natl Acad Sci 1986; 83: 792-6. [28] Semenknovich C, Ostlund R. Estrogens induce low-density lipoprotein receptor activity and decrease intracellular cholesterol in human hepatoma cell line Hep G2. Biochem 1987; 26: 4987-4992. [29] Kurosawa T, Kusanagi M, Yamasaki Y, Senga Y, Yamamoto T. New mutant rabbit strain with hypercholesterolemia and atherosclerotic lesions produced by serial inbreeding. Lab Anim Sci 1995; 45: 385-392.
346 | P a g e M a r c h 0 7 , 2 0 1 4
[13] Rosamond W, Flegal K, Friday G, Furie K, Go A, Greenland K, Haase N, Ho M, Howard V, Kissela B, Kittner S, LloydJones D, McDermott M, Meigs J, Moy C, Nichol G, O’Donnell CJ, Roger V, Rumsfeid J, Sorlie P, Steinberger J,Thom T, Wasserthiel-Smoller S, Hong Y and for the merican Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2007; 115: e69-171. [14] Bronzert TJ, Brewer HB. New micromethod for measuring cholesterol in plasma lipoprotein fractions. Clin Chem 1977; 23: 2089-2098. [15] Folch BJ, Lees M, Sloanestanley GH. A simple method for the isolation and purification of total lipids from animal tissues. J Biol Chem 957; 226: 497-509. [16] Chirgwin JM, Przybyla AE, MacDonald RJ, RutterWJ. Isolation of biologically active ribonucleic acid from sources enriched in ribonuclease. Biochemistry 1979; 18: 5294–9. [17] Yamamoto T, Bishop RW, Brown MS, Goldstein JL, Russell DW. Deletion in cysteine-rich region of LDL receptor impedes transport to cell surface in WHHL rabbit. Science 1986; 232: 1230-7. [18] Kita T, Nagano Y, Yokode M, Ishii K, Kume N, Ooshima A, Yoshida H, Kawai C. Probucol prevents the progression of atherosclerosis in Watanabe heritable hyperlipidemic rabbit, an animal model for familial hypercholesterolemia. Proc Natl Acad Sci USA 1987; 84: 5928-5931. [19] Walsh BW, Schiff I, Rosner B, Greenberg L, Ravnikar V, Sacks F. Effects of postmenopausal estrogen replacement on the concentrations and metabolism of plasma lipoproteins. N Engl J Med 1991; 325: 1196–1204. [20] Ogita H, Node K, Kitakaze M. The role of estrogen and estrogen-related drugs in cardiovascular diseases. Curr Drug Metab 2003; 4: 497–504. [21] Wren BG. The effect of estrogen on the female cardiovascular system. Med J Aust 1992; 157: 204–8. [22] Chao Y, Windler EH, Chen GC, Havel RJ. Hepatic catabolism of rat and human lipoproteins in rats treated with 17alpha-ethinyl estradiol. J Biol Chem 1979; 254: 11360–6. [23] Roach PD, Noel S-P. Solubilisation of the 17-alpha ethinyl estradiol-stimulated low density lipoprotein receptor of male rat liver. J Lipid Res 1985; 26: 713–720. [24] Ma PTS, Yamamoto T, Goldstein JL, Brown MS. Increased mRNA for low density lipoprotein receptor in livers of rabbits treated with 17・-ethinyl estradiol. Proc Natl Acad Sci USA 1986; 83: 792–6. [25] Ferreri F, Naito NK. Effect of estrogens on rat serum cholesterol concentrations: Consideration of dose, type of estrogen and treatment duration. Endocrinol 1978; 102: 1621–7. [26] Owen AJ, Roach PD, Abbey M. Regulation of Low-Density Lipoprotein Receptor Activity by Estrogens and Phytoestrogens in a HepG2 Cell Model. Ann Nutr Metab 2004; 48: 269-275. [27] Ma P, Yamamoto T, Goldstein J, Brown MS. Increased mRNA for low density lipoprotein receptor in livers of rabbits treated with 17 alpha-ethinyl estradiol. Proc Natl Acad Sci 1986; 83: 792-6. [28] Semenknovich C, Ostlund R. Estrogens induce low-density lipoprotein receptor activity and decrease intracellular cholesterol in human hepatoma cell line Hep G2. Biochem 1987; 26: 4987-4992. [29] Kurosawa T, Kusanagi M, Yamasaki Y, Senga Y, Yamamoto T. New mutant rabbit strain with hypercholesterolemia and atherosclerotic lesions produced by serial inbreeding. Lab Anim Sci 1995; 45: 385-392.
Downloads
Published
2014-03-07
How to Cite
Iizuka, A., Yoshie, F., Iizuka, M., Yamaguchi, H., Komatsu, Y., & Kondo, K. (2014). Effects of dietary hypercholesterolemia on plasma lipids levels male and female Japanese white and heterozygous Kurosawa-Kusanagi hypercholesterolemic rabbits. JOURNAL OF ADVANCES IN BIOLOGY, 4(2), 342–350. https://doi.org/10.24297/jab.v4i2.5573
Issue
Section
Articles
License
All articles published in Journal of Advances in Linguistics are licensed under a Creative Commons Attribution 4.0 International License.
