Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 24 miniature swine (Sus scrofa) were fed with two diets of 9% fat content, differing only in the quality of the fat source (sunflower oil and olive oil). Two groups of animals were fed for a 12-week period, and the other two groups were fed for a 50-week period. After the two experimental periods, the influence of the dietary fat on serum lipids and protein and fatty acid composition of isolated LDLs was studied. In the short term, the serum cholesterol level was slightly higher in the olive oil group but, with the time of adaptation to the diet, serum levels of TC, FC and PL increased significantly in the sunflower group. In the long term, LDL and HDL were also significantly higher in the sunflower group when compared to the monounsaturated diet. In the sunflower group, PROT/TC and PROT/LIP ratios decreased significantly with the experimental period, while in the olive oil group they increased, due to the decrease in EC and TG fractions. The LDL particle in the olive group contained fewer saturated fatty acids and more monounsaturated fatty acids, specially oleic acid, than the LDL in the sunflower group. The changes found in chemical and fatty acid compositions of LDL, according to the saturation degree of the predominant fat of the diet, could alter its cellular metabolism.
Comp Biochem Physiol B Biochem Mol Biol 1995 Jun
PMID:The influence of dietary fat source (sunflower oil or olive oil) on LDL composition and serum lipid levels in miniature swine (Sus scrofa). 759 84

Benzodiazepines affect steroidogenesis in at least four ways depending on concentration and adrenocortical cell type. Firstly, at micromolar concentrations, they inhibit steroidogenic enzymes. Competition for microsomal 17- and 21-hydroxylase activity explains the inhibition of ACTH-stimulated aldosterone and cortisol synthesis by diazepam and midazolam. At slightly higher concentrations, we have evidence that 11 beta-hydroxylase activity is also inhibited. Secondly, at sub-micromolar concentrations, calcium influx is inhibited. T-type and L-type calcium channels appear to be blocked, this impairs signal response coupling and, in particular, decreases angiotensin- and K(+)-stimulated aldosterone synthesis in zona glomerulosa cells. Thirdly, the mitochondrion of steroidogenic tissues is a sensitive site for the stimulatory effects of benzodiazepines. Aldosterone synthesis from added HDL-cholesterol by cultured bovine zona glomerulosa cells is stimulated by diazepam, RO5-4864 and PK11195. The fourth site of benzodiazepine's effect on steroidogenesis is particular to zona glomerulosa cells. In addition to cholesterol side chain cleavage, the final part of the aldosterone biosynthetic pathway, the conversion from deoxycorticosterone is controlled. Although high micromolar concentrations of diazepam appear to be inhibitory, lower nanomolar concentrations stimulate the synthesis of aldosterone from added deoxycorticosterone. In vivo, a fifth site of benzodiazepine activity may influence plasma steroid concentrations. Competition between steroids and benzodiazepines for hepatic clearance enzymes may affect half lives of both drugs and hormones.
J Steroid Biochem Mol Biol 1995 Jun
PMID:Regulation of adrenocortical steroidogenesis by benzodiazepines. 762 20

The effects of feeding two levels of rice bran oil (RBO) on the growth, lipid parameters, and fatty acid composition of the plasma and liver of rats (Wistar strain) were compared with those produced on animals which had been fed the same levels of peanut oil (PNO). The control animals were fed synthetic diets containing 5 and 20% peanut oil (PNO) and the experimental groups were fed similar diets, containing the same level of rice bran oil (RBO). There was no significant difference with respect to the organ weights between the control and the experimental groups. In general, groups fed 20% oil gained more weight than groups fed 5% oil. The animals which received rice bran oil in their diet had, in general, comparatively lower levels of cholesterol, triglycerides and phospholipids. On the other hand, animals receiving 20% rice bran oil in their diet, showed an increase of 20% in high density lipoproteins (HDL-C), within 18 weeks (p < 0.05), when compared to the animals fed with peanut oil. Similarly, low density lipoprotein cholesterol (LDL-C) and very low density lipoprotein cholesterol (VLDL-C) were lower in RBO-fed groups, than in the PNO-fed groups. There was, however, no significant differences in the cholesterol/phospholipid (C/P) ratio of the two groups. Analysis of plasma and of liver fatty acids indicated, in a general way, the type of fat consumed. There were no significant difference in the P/S ratio, nor any in the oleic/linoleic, oleic/stearic, palmitoleic/palmitic, oleic/palmitic, and oleic/palmitoleic ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Cell Biochem 1995 May 10
PMID:Effect of long term feeding of rice bran oil upon lipids and lipoproteins in rats. 765 79

The biosynthetic pathway of the CoQ polyisoprenoid side chain, starting from acetyl-CoA and proceeding through mevalonate and isopentenylpyrophosphate, is the same as that of cholesterol. We performed this study to evaluate whether vastatins (hypocholesterolemic drugs that inhibit HMG-CoA reductase) modify blood levels of ubiquinone. Thirty-four unrelated outpatients with hypercholesterolemia (IIa phenotype) were treated with 20 mg of simvastatin for a 6-month period (group S) or with 20 mg of simvastatin plus 100 mg CoQ10 (group US). The following parameters were evaluated at time 0, 45, 90, 135 and 180 days: total plasma cholesterol (TC), HDL-cholesterol, LDL-cholesterol (LDL-C), triglycerides (TG), apo A1, apo B and CoQ10 in plasma and platelets. In the S group, there was a marked decrease in TC and LDL-C (from 290.3 mg/dl to 228.7 mg/dl for TC and from 228.7 mg/dl to 167.6 mg/dl for LDL-C) and in plasma CoQ10 levels from 1.08 mg/dl to 0.80 mg/dl. In contrast, in the US group we observed a significant increase of CoQ10 in plasma (from 1.20 to 1.48 mg/dl) while the hypocholesterolemic effect was similar to that observed in the S group. Platelet CoQ10 also decreased in the S group (from 104 to 90 ng/mg) and increased in the US group (from 95 to 145 ng/mg). This study demonstrates that simvastatin lowers both LDL-C and apo B plasma levels together with the plasma and platelet levels of CoQ10, and that CoQ10 therapy prevents both plasma and platelet CoQ10 decrease, without affecting the cholesterol lowering effect of simvastatin.
Mol Aspects Med 1994
PMID:Exogenous CoQ10 supplementation prevents plasma ubiquinone reduction induced by HMG-CoA reductase inhibitors. 775 30

Plasma coenzyme Q10 (CoQ10) is currently assayed in our laboratory for its well-known diagnostic meaning; in fact plasma CoQ10 levels are inversely related to metabolic demand. Definite levels of CoQ10 are also found in white and red blood cell components, as well as in platelets. Plasma and erythrocyte CoQ10 has a well assessed antioxidant role, which was demonstrated through a series of experiments. Erythrocytes previously enriched with exogenous CoQ10 were found more resistant to a hemolysis induced by a free radical initiator. Several enzymatic activities of erythrocyte ghosts were also protected by different side chain CoQ homologues, both when reduced and, although at a lesser extent, in the oxidized state. CoQ was not effective in preventing metal-catalyzed oxidation of erythrocyte membrane enzymes, and this effect is likely to be due to lack of interaction of CoQ with the metal target. Moreover CoQ was able to protect isolated enzymes and erythrocyte membrane bound enzymes from the inactivating effect of free radicals generated by water sonolysis or radiolysis. As far as plasma lipoproteins are concerned it is well known that LDL isolated from healthy volunteers supplemented with CoQ10 are more resistant to peroxidation induced by an azoinitiator. We started to systematically investigate CoQ10 and vitamin E levels in isolated human LDL and HDL. Both CoQ10 and vitamin E concentrations, referred to protein, were found higher in LDL than in HDL. Susceptibility to exogenously applied peroxidation did not correlate with the endogeneous content of the two antioxidants, possibly on the basis of different lipid content of these lipoproteins.
Mol Aspects Med 1994
PMID:Metabolic implications of coenzyme Q10 in red blood cells and plasma lipoproteins. 775 46

The aim of the present study was to investigate the regulation of the apoAI gene by dietary saturated fat and cholesterol. Saturated fatty acids and cholesterol raise low density- and high density lipoprotein particles in humans. Increased LDL is attributed to the down-regulation of LDL-receptor gene, but the mechanism of increased plasma HDL levels is unknown. To study the mechanism of HDL elevation by saturated fat, male rats and male mice were employed as animal models, since they also raise their plasma HDL levels when fed high lipid diets. Animals were divided in four groups and fed the following diets: control (5% corn oil); high cholesterol (0.5%); high fat (20% coconut oil); and high fat plus cholesterol diets. The high cholesterol diet did not alter plasma and HDL-cholesterol levels. However, the high fat diet increased HDL levels by 20% in rats and 55% in mice. A combination of saturated fat and cholesterol diet raised plasma HDL levels by 36 and 67% in rats and mice, respectively. Plasma apoAI levels increased parallel to HDL concentrations. Mechanism of HDL elevation by saturated fat was investigated. Hepatic and intestinal apoAI mRNA did not change with any of the test diets in mice. Rat hepatic apoAI mRNA was also unchanged by the high cholesterol diet, but was decreased on high fat and fat-cholesterol combination diets. These results suggest that transcriptional regulation of the apoAI gene was not responsible for increased plasma apoAI and HDL. The translational efficiency of apoAI on isolated polysomes was also measured, and it was found that apoAI synthesis increased about 20% on high fat and fat-cholesterol combination diets. This partially explains the elevated levels of plasma HDL. Additional regulation through impaired catabolism of HDL particles by high fat diet feeding may be another pathway for increased HDL levels. Unlike apoAI mRNA, the mRNA of other HDL apoproteins, apoAII and apoAIV, were increased by high fat and combination diet feeding. These results suggest that saturated fatty acids regulate plasma HDL levels by translational and posttranslational mechanisms.
Biochem Mol Biol Int 1994 Sep
PMID:Saturated fatty acid, but not cholesterol, regulates apolipoprotein AI gene expression by posttranscriptional mechanism. 784 50

The objectives of this study were to establish the effects of high-oleic sunflower oil (HOSO) and beef tallow on tissue fatty acids and stearoyl-CoA desaturase activities in swine; and to compare effects of HOSO and tallow on swine plasma triglycerides and lipoprotein-cholesterol fractions. Sixteen gilts were divided into two groups: eight fed a control diet containing 10 g/100 g beef tallow, and eight fed a diet containing 10 g/100 g HOSO. Plasma samples were obtained before feeding began and at 4 weeks and 8 weeks of dietary treatment. Samples were obtained from longissimus dorsi muscle, liver, adipose and duodenal mucosa for the measurement of fatty acid composition and stearoyl-CoA desaturase activity. The HOSO diet increased (P < 0.05) the concentrations (mumol/g wet weight of tissue) of 18:1 and 18:2 (n-6) in adipose tissue. In muscle from pigs fed the HOSO diet, concentrations of 14:0, 16:0, 16:1, 18:0, 18:1, and 18:2 (n-6) decreased (P < 0.05) relative to muscle from pigs fed the beef tallow diet; only 14:0 and 16:1 were reduced in liver by the HOSO diet. Stearoyl-CoA desaturase specific activity [(pmol 7 min-1 mg-1 microsomal protein)] was 40 percent lower, and activity expressed as pmol 7 min-1 g-1 tissue) was 20 percent lower, in adipose tissue of pigs fed HOSO (P < 0.05). No differences due to dietary treatment were observed for desaturase activity from muscle, liver or intestinal mucosa. Plasma triglycerides declined steadily in the tallow-fed pigs, possibly reflecting the lower percentages of liver 18:0 and 18:1 acids, relative to the HOSO-fed pigs. The animals responded similarly to the addition of fat (beef tallow or HOSO) to their diets with increased (P < 0.05) plasma total, LDL- and HDL-cholesterol by 4 weeks of treatment. Total cholesterol, LDL-, VLDL- or HDL-cholesterol were not different between pigs fed beef tallow or HOSO. Thus, differences in fatty acid composition of the diets were sufficient to alter tissue fatty acid composition and adipose tissue desaturase activity, but insufficient to alter plasma lipoprotein cholesterol.
Comp Biochem Physiol B Biochem Mol Biol 1995 Jan
PMID:Lipid metabolism in pigs fed beef tallow or high-oleic acid sunflower oil. 785 42

In this study the role of high density lipoproteins in lipoprotein peroxidation process was investigated. Under basal conditions, HDL isolated from human plasma or from total lipoprotein fraction (density > 1.21) using precipitation technique carried nearly 35-40% of the total plasma fatty acid peroxidation product (measured as malonaldehyde, MDA). HDL associated MDA was reduced to < 20% when HDL was isolated by ultracentrifugation from plasma treated with Cu++. Under these conditions, 45% of the cholesterol peroxidation products (oxysterols) were associated with HDL. HDL isolated from Cu++ treated plasma significantly lost its ability to inhibit LDL peroxidation. These results suggest that HDL plays an important role in lipid peroxidation a) by carrying significant amounts of cholesterol and lipid peroxidation products, and b) its ability to inhibit LDL oxidation is compromised when HDL itself is oxidized.
Biochem Mol Biol Int 1994 Jul
PMID:Significant association of lipid peroxidation products with high density lipoproteins. 798 57

The study of polymorphisms of human apolipoprotein AI/CIII/IV gene cluster in the Moscow population was carried out using of methods of polymerase chain reaction and restriction. Polymorphisms of apolipoprotein AI/CIII/AIV gene cluster detected with SacI, PstI, PvuII, MspI have been investigated to search for their possible relation to the following quantitative lipid parameters: total cholesterol, HDL cholesterol, triglycerides, apolipoproteins AI, apolipoproteins B. It has been determined that in groups of individuals with increased cholesterol level the frequencies of uncommon alleles at the MspI, SacI, PvuII sites were significantly higher than in controls. Our results show that in groups with increased triglyceride level the frequency of uncommon alleles at the MspI and SacI sites was higher than in controls. Individuals with elevated apolipoprotein B and ratio of apolipoproteins B/AI > 1 have significantly higher frequency of uncommon alleles at the SacI and PvuII sites and uncommon alleles at the PvuII site, respectively. There was no statistically significant correlation between polymorphism at PstI site and lipid level variation. It has been established, by constructing DNA haplotypes, that the presence of particular haplotypes containing an uncommon allele at the PvuII and SacI sites, PvuII and MspI sites, MspI and SacI sites, PvuII and PstI sites, SacI and PstI sites is associated with lipid disorders, and may be associated with development of atherosclerosis.
Mol Biol (Mosk)
PMID:[Connection of polymorphic alleles of the gene cluster AI/CIII/AIV with disturbed lipid metabolism]. 814 52

Serum triacylglycerol (TG) concentration is markedly elevated in Nagase analbuminemic rats (NAR) as compared to Sprague-Dawley rats (SDR) and reflects a high level of mainly VLDL. Hepatic production of triacylglycerol, as measured by the Triton-WR1339 infusion technique of impairing TG removal from blood, and plasma metabolic rate of pulse-infused [125I]apo VLDL, were higher in NAR. However, contrary to previous reports, this elevated TG production could not be controlled by previous treatment of NAR with (i) bovine albumin infused intra-arterially or into the peritoneal cavity, or with (ii) dextran (Mol.wt. 73,500) injected intraperitoneally. Albumin administration expanded the plasma volume and could explain the apparent reduction of blood lipids found by others. Nonetheless, intraperitoneal dextran, as compared to saline, reduced the plasma cholesterol concentration regardless of the variation in the hematocrit level and thus, by raising the osmotic pressure of blood might regulate the metabolism of cholesterol-rich lipoproteins such as LDL and HDL in NAR.
 ...
PMID:Nagase analbuminemic rats have faster plasma triacylglycerol and VLDL synthesis rates. 815 19


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