Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased morbidity and mortality from atherosclerotic vascular disease were observed in subjects with slightly elevated urinary albumin excretion rate (UAER), known as microalbuminuria. Therefore, the association between microalbuminuria and established atherogenic risk factors was studied in clinically healthy subjects. All healthy 40-65 year-old participants with microalbuminuria, examined within the first 21 months of The Copenhagen City Heart Study, were invited, and 28 were studied. An age- and sex-matched group of 60 randomly chosen subjects with normoalbuminuria served as control. Microalbuminuria was defined as a UAER of 6.6-150 micrograms/min, and normoalbuminuria as a UAER < or = 6.6 micrograms/min. In the microalbuminuric group, systolic and diastolic blood pressures were both elevated (mean (95% C.I.) 128 (123-134) vs. 119 (116-122) mmHg; P = 0.005, and 75 (71-78) vs. 69 (67-71) mmHg; P = 0.008, respectively), and serum apolipoprotein (apo) A-1 concentration was lower (1.30 (1.20-1.37) vs. 1.42 (1.36-1.47) milligrams; P = 0.02) in comparison with the normoalbuminuric group. Furthermore, serum HDL-cholesterol concentration tended to be lower, whereas body weight, body mass index and fasting serum insulin concentration were slightly elevated in the microalbuminuric group but not statistically significant. It is concluded that microalbuminuria in clinically healthy subjects is associated with increased levels of atherogenic risk factors. This may contribute to the increased vascular morbidity and mortality observed in these individuals.
Atherosclerosis 1995 Jan 20
PMID:Atherosclerotic risk factors are increased in clinically healthy subjects with microalbuminuria. 777 83

Jejunoileostomy effects on blood lipids and cardiovascular system were investigated in obese patients. They were found to lose 30% of their body mass within 6 postoperative months with parallel reduction in concentrations of total cholesterol, triglycerides, LDL and VLDL cholesterol and apoprotein B. These changes persisted for 4.5 years of the follow-up. The surgery in males has a more pronounced effect on blood lipids than in females. Significant changes were not registered in post- and preoperative levels of HDL cholesterol and apolipoprotein A-1. Jejunoileostomy promoted a fall in blood pressure, a rise in exercise tolerance, alleviation of atherosclerosis symptoms.
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PMID:[Jejunoileal bypass in the prevention and treatment of clinical manifestations of atherosclerosis in patients with morbid obesity]. 785 13

Alcohol intake and exercise have both been found to be related to increased plasma levels of high density lipoprotein cholesterol (HDLC). Exercise training results in decreased postprandial lipemia, and clearance rate of infused lipids is related to plasma lipoprotein levels in physically active men. The effect of alcohol intake on plasma triglyceride (TG) clearance has not been studied in relation to the exercise status of subjects. Plasma TG change over 8 h was determined following a liquid fatty meal in 14 male habitual runners (R) and 13 physically inactive men (I) after 3 weeks of alcohol abstinence and 3 weeks of drinking approximately 41 g (1.44 oz) of ethanol per day. Fasting total cholesterol and apolipoprotein A-1 (apo A-1) were not different between groups, but TG was lower and HDLC, HDL2C, and HDL3C were higher in the runners. After abstinence, I had slower TG clearance (P = 0.07) compared with R; with alcohol, TG clearance was unchanged in R, but was significantly retarded in I. With alcohol, both groups had increased HDLC levels, but this mainly was due to an increase in HDL3C in R and HDL2C in I; apo A-1 increased similarly in both groups and fasting TG increased significantly only in I. Alcohol-induced increases in postprandial lipemia and retardation of TG clearance appear to occur in inactive, but not exercise-trained subjects and the effect of alcohol on plasma HDL subfractions may differ between these groups.
Atherosclerosis 1993 Apr
PMID:Effect of alcohol and exercise on postprandial lipemia and triglyceride clearance in men. 831 61

Genetic dimorphism of the cerumen was studied in a random sample from the Lithuanian population (N = 253), among the patients with the most atherosclerotic risk, from different age groups (N = 276) and in a cohort of long-living (N = 117). Simultaneously, the levels of apolipoprotein (apo- A-1, B, E) were determined in blood sera of the males-donors, long-living and elderly individuals depending on the phenotypes for ear wax consistency. The prevalence of frequency of the w gene for humid cerumen in children suffering from the insulin-dependent diabetes mellitus was found as compared with populational sample--0.8293 and 0.6024, respectively (P < 0.002). On the contrary, essential increase in frequency of the d gene responsible for dry cerumen in long living was found as compared with the control--0.5311 and 0.3976, respectively (P < 0.01). An absence of differences in the concentrations of w and d alleles among the patients with coronary artery atherosclerosis and the populational control indicated that the genetic characters under study exerted no marked change in incidence of atherogenesis. However, the ratio apoB/apoA-1 proved higher in the donors with humid ear wax than in those with the dry variant under P < 0.06, which can stimulate this disease. The results of this study support the statement that low level of apoB and especially apoB/apoA-1 may be one of the longevity markers.
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PMID:[Interrelation of genetic dimorphism of ear wax and the level of apolipoproteins with atherogenesis and longevity in the Lithuanian population]. 848 62

Apolipoprotein A-1 (apoA-1) in complex with high-density lipoprotein is critically involved in the transport and metabolism of cholesterol and in the pathogenesis of atherosclerosis. We reexamined the thermal unfolding of lipid-free apoA-1 in low-salt solution at pH approximately 7, by using differential scanning calorimetry and circular dichroism. At protein concentrations <5 mg/ml, thermal unfolding of apoA-1 is resolved as an extended peak (25 degrees C-90 degrees C) that can be largely accounted for by a single reversible non-two-state transition with midpoint Tm 57 +/- 1 degree C, calorimetric enthalpy deltaH(Tm)= 200 +/- 20 kcal/mol (1 kcal = 4.18 kJ), van't Hoff enthalpy deltaHv(Tm) approximately 32.5 kcal/mol, and cooperativity deltaHv(Tm)/deltaH(Tm) approximately 0.16. The enthalpy deltaH(Tm) can be accounted for by melting of the alpha-helical structure that is inferred by CD to constitute approximately 60% of apoA-1 amino acids. Farand near-UV CD spectra reveal noncoincident melting of the secondary and tertiary structural elements and indicate a well-defined secondary structure but a largely melted tertiary structure for apoA-1 at approximately 37 degrees C and pH 7. This suggests a molten globular-like state for lipid-free apoA-1 under near-physiological conditions. Our results suggest that in vivo lipid binding by apoA-1 may be mediated via the molten globular apolipoprotein state in plasma.
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PMID:Thermal unfolding of human high-density apolipoprotein A-1: implications for a lipid-free molten globular state. 861 Jan 56

The development of atherosclerosis is often associated with altered concentrations of systemic lipoproteins, which are determined by the concentration and/or activity of three groups of different proteins, i.e. apolipoproteins (apo), enzymes, and receptors. The effects of diet or therapeutic interventions on lipid metabolism are mediated by changes in activity or concentrations of these three components. Fibrates have been shown to activate nuclear receptors belonging to the steroid hormone receptor super-family, termed peroxisome proliferator activated receptor (PPAR). These activated PPARs are potent transcription factors which influence the expression of several target genes implicated in lipoprotein homeostasis, e.g. LPL, apo C-III and apo A-1. Fibrates decrease apo C-III transcription and increase LPL production via these PPARs resulting in a profound hypotriglyceridaemic effect. Apolipoproteins and enzymes are important in governing lipid metabolism, thus therapeutically altering the expression of these genes constitutes an efficient therapeutic option.
Atherosclerosis 1996 Jul
PMID:Transcriptional control of triglyceride metabolism: fibrates and fatty acids change the expression of the LPL and apo C-III genes by activating the nuclear receptor PPAR. 883 13

Seasonal variation in the plasma lipids and lipoproteins is reported in the literature. Whether this variation is the result of changes in diet or other factors has not been adequately addressed. We investigated the effects of a controlled diet on the seasonal variation in the levels of plasma lipids and apolipoproteins and also on the excretion of urine metabolites of TXA2 and PGI2 in healthy males. Two well-controlled diet studies were conducted to evaluate effects of dietary fatty acids on plasma lipids (Studies 1 and 2; n = 33) and eicosanoid excretion (Study 2 only; n = 15). Participants consumed whole-food test diets in a randomized, four-period crossover design during each 26-day experimental period. A non-intervention control group also participated in each study (Study 1, n = 12; Study 2, n = 11). Blood was collected monthly and analyzed for plasma lipids and apolipoproteins A-1 (Apo A-1) and B100 (Apo B). Twenty-four hour urine samples were collected monthly only in Study 2 and analyzed for TXB2 and 6-keto-PGF1 alpha by RIA. Seasonal fluctuations were observed in all subjects in plasma Apo A-1 (zenith = July, with 95% CI June-July; P < 0.05) and Apo B (zenith = October, 95% CI September-November, P < 0.05). Although there was no significant variation in plasma cholesterol levels, the increase in Apo B is consistent with an increase in LDL particle number during the fall/winter. Additionally, excretion of both eicosanoid metabolites and the ratio of 6-keto-PGF1 alpha/TXB2 was markedly elevated in July (95% CI June-July, P < 0.001). Three seasonal fluctuations were observed both in participants who consumed a highly-controlled experimental diet and in the non-intervention controls. Thus, these results suggest a diet-independent seasonal variation in parameters thought to be involved in coronary heart disease risk status. An understanding of these variations is important not oly for clinical evaluation and metabolic study design issues, but more importantly, to clarify their clinical significance with the seasonal incidence of CHD events.
Atherosclerosis 1996 Sep 27
PMID:Seasonal variation in parameters related to coronary heart disease risk in young men. 887 40

We tested the ability of remnant-like particles (RLP) from NIDDM patients to stimulate cholesteryl ester synthesis in human monocyte-derived macrophages. Six NIDDM patients were studied together with 7 non-diabetic subjects. All had apolipoprotein (apo) E3/3 phenotype. RLP were isolated using an immunoaffinity gel mixture of anti apo B-100 and anti apo A-1 monoclonal antibodies coupled to Sepharose 4B. Plasma levels of triglyceride, total cholesterol (chol) and high density lipoprotein-chol were not statistically different, but plasma levels of RLP-chol were significantly (p < 0.05) higher in NIDDM patients (10.5 +/- 2.2 mg/dl) than in non-diabetic controls (5.0 +/- 1.7 mg/dl). The effects of RLP from NIDDM patients on macrophage cholesteryl ester synthesis were estimated. 14C-oleate incorporation into cholesteryl esters in macrophages was significantly (p < 0.01) higher in NIDDM patients with apo E3/3 (0.326 +/- 0.037 nmole/mg cell protein) than in non-diabetic controls with apo E3/3 (0.181 +/- 0.011 nmole/ mg cell protein). It is suggested that RLP from NIDDM play a role in the accumulation of cholesteryl esters and are one of the risk factors for the acceleration of atherosclerosis in NIDDM.
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PMID:Remnant-like particles (RLP) from NIDDM patients with apolipoprotein E3/3 phenotype stimulate cholesteryl ester synthesis in human monocyte-derived macrophages. 889 73

A low HDL cholesterol level is frequently but not consistently associated with inefficient postprandial fat clearance. We studied triglycerides, retinyl palmitate and squalene and apolipoprotein B-48 after a fat loading test in one subject heterozygous for a novel point mutation of apolipoprotein A-I (A-IFIN, Leu 159-->Arg) and low HDL cholesterol level without coronary artery disease, and in 16 healthy controls with the same apolipoprotein E phenotype, 3/3, as the proband. HDL cholesterol and apolipoprotein A-I levels were 0.32 mmol/l and 57 mg/dl in the proband, and 1.29 +/- 0.12 mmol/l (mean +/- S.E.) and 126 +/- 4 mg/dl in the controls. The peak concentration for triglycerides in plasma, chylomicrons and VLDL occurred at 4 h both in the case and controls. However, the peak concentrations for retinyl palmitate and squalene in chylomicrons and VLDL were delayed to 12 h in the proband compared with 4 and 9 h in the controls. The peak of apolipoprotein B-48 occurred at 6 h in the proband and at 4 h in the controls, so that triglycerides, apolipoprotein B-48 and retinyl palmitate and squalene peaked differently. After 24 h, retinyl palmitate, squalene, and apolipoprotein B-48 had returned to the baseline levels. The results show for the first time an impaired postprandial lipoprotein removal in a case heterozygote with moderately low HDL cholesterol due to an apolipoprotein A-1 mutation not associated with coronary artery disease.
Atherosclerosis 1996 Dec 20
PMID:Delayed postprandial retinyl palmitate and squalene removal in a patient heterozygous for apolipoprotein A-IFIN mutation (Leu 159-->Arg) and low HDL cholesterol level without coronary artery disease. 912 14

The development of dyslipoproteinemia is to a large extent genetically determined. The mutations in gene controlling receptor to lipoproteids of low density, the genes Apo B, Apo A-1, and Apo E have a dominant role in the disturbance of lipid metabolism. The development of atherosclerosis at young age is apparently associated with the mutations in gene of receptors, in the gene Apo B and some mutations in a cluster of the genes A-I--CIII--AIV.
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PMID:[The genetic bases of the lipid metabolic disorders in atherosclerosis]. 928 Dec 5


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