Effects of additions of amino acids to a 20% casein diet on serum cholesterol (Ch) were studied in hypothyroid and hepatoma-bearing rats with endogenous hypercholesterolemia as well as in normal rats. In normal Wistar rats, methionine (Met) was hypercholesterolemic at the "nutritional" level (0.2-0.4%), but hypocholesterolemic at the "excess" level (1.2-2.4%). In Wistar rats with hypothyroidism induced by thiouracil, the addition of excess (1.2%) Met to the 20% casein diet reduced an endogenous hypercholesterolemia due to hypothyroidism by suppressing an elevation in (VLDL + LDL)-Ch with no significant influence on HDL-Ch. In Donryu rats received a subcutaneous implantation of AH109A cells (an ascites hepatoma line), either 1.2% Met, 1.2% cystine (Cys), or 1.2% Met and 2.5% glycine (Gly) in combination improved a hepatoma-induced hypercholesterolemia and abnormal serum lipoprotein profiles by suppressing a hepatoma-induced increase in (VLDL + LDL)-Ch. From Ch turnover studies in hepatoma-bearing rats, an impaired catabolism of Ch in the liver was suggested to be one cause for the hepatoma-induced elevation in (VLDL + LDL)-Ch. One of the dietary manipulations. met and Gly in combination (Met + Gly), was found to improve the impaired Ch catabolism, this leading to a reduction of the (VLDL + LDL)-Ch level by Met + Gly in hepatoma-bearing rats.
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http://dx.doi.org/10.3177/jnsv.36.supplementii_s165 | DOI Listing |
Oxid Med Cell Longev
July 2022
Molecular Physiology Division, Zoology Department, Faculty of Science, Beni-Suef University, P.O. Box 62521, Beni Suef, Egypt.
Atherosclerosis is a disease in which plaque builds up inside arteries. Cinnamaldehyde (Ci) has many biological properties that include anti-inflammatory and antioxidant activities. Thus, this study was designed to explore the protective effect of Ci against atherosclerosis induced by a high-fat diet (HFD) in Wistar rats.
View Article and Find Full Text PDFBull Exp Biol Med
December 2018
Research Centre for the Problems of Family Health and Human Reproduction, Irkutsk, Russia.
Predictive models of comorbidity, dyslipidemic disorders and essential arterial hypertension, in Russian adolescents aged 12 to 18 years (mean 15.48±1.53) were formulated with consideration for biochemical (lipid profiles) and genetic parameters (carrier state of gene polymorphic variants of apolipoprotein genes ApoA1 (-75G/A and +83C/T), ApoB (Ins/Del), ApoC3 (S1/S2), and ApoE (ε2/ε3/ε4).
View Article and Find Full Text PDFEnviron Toxicol
December 2018
Laboratory of Animal Eco-physiology, Faculty of Sciences, Sfax University, Sfax, Tunisia.
Environmental pollutants, particularly lead, pose a serious threat to human and animal health that causes disturbances of several functions, including hepatotoxicity. Therefore, the search for a new treatment that could safely and effectively block or reverse liver injuries remains a challenge. This study was carried out to investigate the protective efficacy of Juglans regia vegetable oil (JRVO) against the hepatotoxicity induced by lead.
View Article and Find Full Text PDFActa Pol Pharm
May 2011
Division of Medicinal and Pharmaceutical Chemistry, Dept. of Pharmaceutical Technology, Jadavpur University, Kolkata-700032, India.
A drug may cause alteration in blood-lipid profile and induce lipid peroxidation phenomena on administration in the body. Antioxidant may play beneficial role to control the negative alteration in lipid profile and lipid peroxidation. In view of this context, the present in vivo study was carried out to evaluate the role of ascorbic acid as antioxidant on netilmicin-induced alteration of blood lipid profile and peroxidation parameters.
View Article and Find Full Text PDFPostepy Hig Med Dosw (Online)
January 2010
Zakład Medycyny Laboratoryjnej Katedra Biochemii Klinicznej, Gdański Uniwersytet Medyczny, Gdańsk.
Dyslipidemia in metabolic syndrome (MS), called the atherogenic triad, includes elevated levels of plasma triglycerides (TGs), low levels of HDL-cholesterol (HDL-CH), and the presence of small dense low-density lipoproteins (sdLDLs) with normal or slightly elevated LDL-CH levels. Insulin resistance drives the increase in the three main sources of TG for VLDL synthesis: fatty-acid flux from adipose tissue, de novo lipogenesis, and uptake of remnant lipoproteins. Overproduction of VLDL, predominantly triglyceride-rich large VLDL1 particles, induces the cascade of events which lead to abnormalities of other plasma lipoproteins.
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