scholarly journals Effects of the whole seed and a protein isolate of faba bean (Vicia faba) on the cholesterol metabolism of hypercholesterolaemic rats

2001 ◽  
Vol 85 (5) ◽  
pp. 607-614 ◽  
Author(s):  
M. Teresa Macarulla ◽  
César Medina ◽  
M. Aránzazu De Diego ◽  
M. Chávarri ◽  
M. Ángeles Zulet ◽  
...  
Keyword(s):  
Vicia Faba ◽  
Faba Bean ◽  
Cholesterol Metabolism ◽  
Reductase Activity ◽  
Protein Isolate ◽  
Experimental Conditions ◽  
Hmg Coa Reductase ◽  
Faecal Excretion ◽  
Whole Seed ◽  
Coa Reductase

The aim of the present work was to analyse the hypocholesterolaemic efficiency of aVicia faba-protein isolate in relation to the intact legume. In addition, the mechanisms underlying the effects of this isolate were investigated. Hypercholesterolaemic rats were divided into three groups (n 10×3) and fed high-fat diets rich in cholesterol-containing casein, whole seeds ofVicia fabaor the protein isolate of faba beans as protein source, for 2 weeksad libitum. The protein isolate was prepared by isoelectric precipitation and spray dried. Analyses of serum, liver and faeces, as well as of the activity of hepatic 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase, were assessed by enzymatic methods. The rats fed onVicia fabadiets showed significantly lower body weights and energy intakes than rats fed on casein diets. The whole-seed diet induced a significant reduction in plasma triacylglycerol. Feeding rats on diets containing faba bean seeds, or the protein isolate, induced a significant decrease in plasma (LDL+VLDL)-cholesterol but not in HDL-cholesterol. Hepatic cholesterol and triacylglycerol were also reduced. The hypocholesterolaemic effects ofVicia fabawere not the result of a reduction in cholesterol synthesis as assessed from HMG-CoA reductase activity, but the result of an increase in steroid faecal excretion. The faba bean-protein isolate obtained under our experimental conditions was useful in improving the metabolic alterations induced by feeding with a hypercholesterolaemic diet compared with casein. The effectiveness of the whole seeds was higher than that of the protein isolate.

scholarly journals Inhibition of HMG-CoA Reductase Activity from Active Compounds of Ginger (Zingiber officinale): In-Silico Study

2021 ◽  
Vol 1 (1) ◽  
pp. 32-38
Author(s):  
Rosario Trijuliamos Manalu ◽  
Imelia Omega Meheda ◽  
Cintya Octaviani
Keyword(s):  
In Silico ◽  
Cholesterol Metabolism ◽  
Raw Materials ◽  
Reductase Activity ◽  
Zingiber Officinale ◽  
Active Compounds ◽  
Hmg Coa Reductase ◽  
Conducting Research ◽  
Main Components ◽  
Coa Reductase

ABSTRAK   Koleterol merupakan salah satu dari lemak tubuh dalam asam lemak bebas dan ester, yang termasuk komponen utama selaput sel otak dan saraf. Namun, tidak jarang kolesterol menjadi penyebab penyakit terutama penyakit jantung yang terus meningkat setiap tahunnya di Indonesia. Sehingga perlu strategi pengobatan yang efektif dan aman dengan melakukan penelitian tanaman Indonesia sebagai upaya kemandirian bahan baku obat. Tujuan dari penelitian ini adalah untuk menentukan aktivitas penghambatan dari senyawa aktif tanaman Jahe pada HMG-KoA reduktase secara in-silico melalui penambatan molekul. Senyawa aktif yang digunakan dalam penelitian ini curcumin, capsaisin, gingerol, paradol, shogaol dilakukan docking molekuler menggunakan software PLANTS dengan tujuan untuk mengetahui score docking dan interaksi kelima senyawa terhadap enzim HMG-KoA reduktase yang berperan terhadap metabolism lemak/kolesterol. Senyawa pembanding yang digunakan adalah simvastatin dan atorvastatin yang merupakan obat lini pertama untuk pengobatan displipidemia. Hasil score docking menunjukkan bahwa kelima senyawa aktif yang digunakan sebagai ligan, menunjukkan score docking yang lebih rendah dibandingkan dengan ligan pembanding, sehingga kelima senyawa aktif ini mampu untuk menghambat biosintesis kolesterol atau kandidat obat baru pengganti simvastatin dan atorvastatin serta berpotensi sebagai dyslipidemia.   ABSTRACT Cholesterol is one of the body's fats in free fatty acids and esters, which are the main components of brain and nerve cell membranes. However, it is not uncommon for cholesterol to be the cause of disease, especially heart disease, which continues to increase every year in Indonesia. So it needs an effective and safe treatment strategy by conducting research on Indonesian plants as an effort to be independent of medicinal raw materials. The aim of this study was to determine the inhibitory activity of the active compound of Ginger plant on HMG-CoA reductase in-silico through molecular anchoring. The active compounds used in this study were curcumin, capsaicin, gingerol, paradol, shogaol. Molecular docking was carried out using PLANTS software with the aim of knowing the docking score and the interaction of the five compounds with the HMG-CoA reductase enzyme that plays a role in fat/cholesterol metabolism. Comparative compounds used are simvastatin and atorvastatin which are first-line drugs for the treatment of dysplipidemia.  

Effect of ethanol on cell growth and cholesterol metabolism in cultured Hep G2 cells

2003 ◽  
Vol 81 (6) ◽  
pp. 379-386 ◽  
Author(s):  
Mónica P Polo ◽  
Margarita G de Bravo ◽  
María JT de Alaniz
Keyword(s):  
Growth Rate ◽  
Cell Growth ◽  
Culture Medium ◽  
Cholesterol Metabolism ◽  
Reductase Activity ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Hmg Coa Reductase ◽  
G2 Cells ◽  
Coa Reductase

The Hep G2 human hepatoma cell line has been recognized as an excellent in vitro human model system. For this reason, this line was used to study the effect of ethanol on HMG-CoA reductase activity concerning cell growth and cholesterol metabolism. Cells were incubated in ethanol-containing medium (0–400 mmol/L) for up to 102 h. Ethanol caused an inhibition in the growth rate and in HMG-CoA reductase activity that could be reverted by the removal of ethanol from the culture medium, indicating no cellular damage. These changes cannot be ascribed to the regulatory effect of cholesterol levels, since its content was not modified either in the cells or in the medium. The addition of mevalonate to the culture medium could not revert the growth rate inhibition evoked by ethanol. Moreover, ethanol produced an increment in the cholesterol efflux in [3H]cholesterol-prelabeled cells. We conclude that the decrease in HMG-CoA reductase activity evoked by ethanol treatment on Hep G2 cells would not be the cause but the consequence of the impairment in cellular growth, since this impairment could not be reverted by the addition of mevalonate to the culture medium.Key words: ethanol, cholesterol, HMG-CoA reductase, hepatoma cells, lipid metabolism.

scholarly journals Effect of lovastatin on acyl-CoA: cholesterol O-acyltransferase (ACAT) activity and the basolateral-membrane secretion of newly synthesized lipids by CaCo-2 cells

1990 ◽  
Vol 272 (2) ◽  
pp. 427-433 ◽  
Author(s):  
N T Kam ◽  
E Albright ◽  
S Mathur ◽  
F J Field
Keyword(s):  
Cholesterol Synthesis ◽  
Cholesterol Metabolism ◽  
Reductase Activity ◽  
Basolateral Membrane ◽  
Fatty Acyl ◽  
Intestinal Cell ◽  
Intact Cells ◽  
Hmg Coa Reductase ◽  
Acat Activity ◽  
Coa Reductase

Lovastatin, a potent competitive inhibitor of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase activity, was used to study the regulation of cholesterol metabolism and the basolateral-membrane secretion of triacylglycerol and cholesterol in the human intestinal cell line CaCo-2. At 0.1 microgram/ml, lovastatin decreased 3H2O incorporation into cholesterol by 71%. In membranes prepared from cells incubated with lovastatin for 18 h, HMG-CoA reductase activity was induced 4-8-fold. Mevalonolactone prevented this induction. In intact cells, lovastatin (10 micrograms/ml) decreased cholesterol esterification by 50%. The reductase inhibitor decreased membrane acyl-CoA:cholesterol O-acyltransferase (ACAT) activity by 50% at 5 micrograms/ml. ACAT inhibition by lavastatin was not reversed by adding excess of cholesterol or fatty acyl-CoA to the assay. Lovastatin, in the presence or absence of mevalonolactone, decreased the basolateral secretion of newly synthesized cholesteryl esters and triacylglycerols. Lovastatin also inhibited the esterification of absorbed cholesterol and the secretion of this newly synthesized cholesteryl ester. Lovastatin is a potent inhibitor of cholesterol synthesis in CaCo-2 cells. Moreover, it is a direct inhibitor of ACAT activity, independently of its effect on HMG-CoA reductase and cholesterol synthesis.

Water-Soluble Compounds fromLentinula edodesInfluencing the HMG-CoA Reductase Activity and the Expression of Genes Involved in the Cholesterol Metabolism

2016 ◽  
Vol 64 (9) ◽  
pp. 1910-1920 ◽  
Author(s):  
Alicia Gil-Ramírez ◽  
Víctor Caz ◽  
Fhernanda R. Smiderle ◽  
Roberto Martin-Hernandez ◽  
Carlota Largo ◽  
...  
Keyword(s):  
Cholesterol Metabolism ◽  
Reductase Activity ◽  
Water Soluble ◽  
Hmg Coa Reductase ◽  
Expression Of Genes ◽  
Coa Reductase

scholarly journals The absolute rate of cholesterol biosynthesis in monocyte-macrophages from normal and familial hypercholesterolaemic subjects

1984 ◽  
Vol 219 (2) ◽  
pp. 461-470 ◽  
Author(s):  
D D Patel ◽  
C R Pullinger ◽  
B L Knight
Keyword(s):  
Cholesterol Synthesis ◽  
Reductase Activity ◽  
Cholesterol Biosynthesis ◽  
Specific Radioactivity ◽  
Density Lipoprotein ◽  
Cellular Protein ◽  
True Rate ◽  
Hmg Coa Reductase ◽  
Coa Reductase ◽  
In Cells

The true rate of cholesterogenesis in cultured monocyte-macrophages was determined from the incorporation of [2-14C]acetate into cholesterol, using the desmosterol (cholesta-5,24-dien-3 beta-ol) that accumulated in the presence of the drug triparanol to estimate the specific radioactivity of the newly formed sterols. It was shown that this procedure could be successfully adapted for use with cultured monocytes despite the accumulation of other unidentified biosynthetic intermediates. In cells maintained in 20% (v/v) whole serum approx. 25% of the sterol carbon was derived from exogenous acetate. Cholesterol synthesis was as high in normal cells as in cells from homozygous familial hypercholesterolaemic (FH) subjects and accounted for 50% of the increase in cellular cholesterol. The addition of extra low-density lipoprotein (LDL) reduced cholesterol synthesis, apparently through a decrease in the activity of 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA reductase). When incubated in lipoprotein-deficient serum some cells did not survive, but those that remained showed a normal increase in protein content; the amount of cellular protein and cholesterol in each well did not increase and cholesterol synthesis was reduced by over 80%. HMG-CoA reductase activity fell less dramatically and the proportion of sterol carbon derived from exogenous acetate increased, suggesting that the low rate of cholesterogenesis with lipoprotein-deficient serum was due to a shortage of substrate. The results indicate that under normal conditions monocyte-macrophages obtain cholesterol from endogenous synthesis rather than through receptor-mediated uptake of LDL, and that synthesis together with non-saturable uptake of LDL provides the majority of the cholesterol required to support growth.

scholarly journals The roles of different protein kinases and of calmodulin in the effects of Ca2+ mobilization on 3-hydroxy-3-methylglutaryl-CoA reductase activity in isolated rat hepatocytes

1991 ◽  
Vol 273 (2) ◽  
pp. 485-488 ◽  
Author(s):  
V A Zammit ◽  
A M Caldwell
Keyword(s):  
Protein Kinase ◽  
Reductase Activity ◽  
Rat Hepatocytes ◽  
Total Activity ◽  
Isolated Hepatocytes ◽  
Isolated Rat Hepatocytes ◽  
Hmg Coa Reductase ◽  
Lysosomal Proteolysis ◽  
Dependent Protein ◽  
Coa Reductase

The roles of protein kinase C, Ca2+/calmodulin-dependent protein kinase and AMP-activated protein kinase in the phosphorylation of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase induced by Ca2(+)-mobilizing conditions in isolated hepatocytes were investigated. Only partial evidence for the involvement of AMP-activated kinase was found. Antagonism of calmodulin action prolonged the decrease in expressed/total activity ratio induced by vasopressin plus glucagon. Protease inhibitors active against Ca2(+)-dependent cytosolic proteases or lysosomal proteolysis did not attenuate the loss of total HMG-CoA reductase induced by glucagon plus vasopressin, but calmodulin antagonists largely prevented this effect.

Differential effects of dietary fat on chick plasma and liver composition and HMG-CoA reductase activity

1999 ◽  
Vol 10 (4) ◽  
pp. 198-204 ◽  
Author(s):  
Mercedes Castillo ◽  
José H Hortal ◽  
Almudena Gil-Villarino ◽  
Purificación Luque ◽  
José Iglesias ◽  
...  
Keyword(s):  
Dietary Fat ◽  
Reductase Activity ◽  
Hmg Coa Reductase ◽  
Differential Effects ◽  
Coa Reductase
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