Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In two inbred strains of rabbits with high or low response of serum cholesterol to dietary cholesterol, binding of rabbit beta-VLDL to hepatic membrane preparations was determined. The objective was to test the hypothesis that after cholesterol feeding, hyperresponders show a more dramatic reduction in hepatic apolipoprotein (apo) B/E receptors, which may explain the development of the high degree of cholesterolemia in these animals. The number of hepatic high affinity receptors for beta-VLDL in hyperresponders fed a diet without added cholesterol was, on average, 20% lower than that in hyporesponders. After the addition of increasing amounts of cholesterol to the diet, liver cholesterol concentrations were elevated to a greater extent in hyper- than in hyporesponsive rabbits. Liver free cholesterol concentrations were negatively associated with maximal binding of beta-VLDL to liver membranes. With increasing liver free cholesterol concentrations, maximal binding was less effectively depressed in hyper- than hyporesponders. We conclude that in the inbred strains of rabbits, hyperresponsiveness to dietary cholesterol is not caused by enhanced depression of hepatic apo B/E receptors.
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PMID:Hyperresponsiveness to dietary cholesterol in inbred rabbits is not associated with enhanced reduction in binding of beta-VLDL to liver membranes. 155 67

Human hepaotoblastoma cells (Hep G2) were cultured with a competitive inhibitor of HMG-CoA reductase, CS-514. The synthesis of cholesterol was markedly inhibited after 1 h preincubation with CS-514. The synthesis and secretion of apolipoprotein (apo) B and A-1, however, were not affected. A long-term incubation (21-24 h) of cells with CS-514 did not change apo B synthesis and secretion, although a slight depression of apo A-1 synthesis was observed. Hep G2 cells were found to secrete LDL- and HDL-like lipoproteins which were poor in cholesterol when cells were incubated with the drug. These results suggest that the modulation of cholesterol synthesis affects neither the synthesis and secretion of apo B and A-1 nor the formation of lipoproteins.
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PMID:The effect of HMG-CoA reductase inhibitor (CS-514) on the synthesis and secretion of apolipoproteins B and A-1 in the human hepatoblastoma Hep G2. 215 11

Diets currently used to produce atherosclerotic lesions in mice are often undefined and cause accumulation of fat in the liver and gallstone formation. Therefore, synthetic low and high fat diets of known composition were formulated in this study. A synthetic diet containing 50% sucrose, 15% cocoa butter, 1% cholesterol, and 0.5% sodium cholate was found to produce a depression in high density lipoprotein cholesterol (HDL-C) and an elevation of very low density lipoprotein (VLDL) and low density lipoprotein cholesterol (LDL-C) in the atherosclerosis-susceptible strain, C57BL/6J. This diet was able to consistently produce aortic lesions and led to a decrease in liver damage and gallstone formation. The synthetic low fat diet did not produce HDL-C levels as high as those found in mice fed chow, but resulted in similar VLDL/LDL-C levels. Lipoprotein and apolipoprotein parameters were compared in C57BL/6J and the atherosclerosis-resistant strain, C3H/HeJ, consuming the synthetic low fat or high fat diets. As reported earlier, when consuming a high fat diet C57BL/6J mice have significantly lower HDL-C and apoA-I levels than C3H/HeJ mice. Further analysis shows that the molar ratio of plasma HDL-C to apoA-I is significantly lower in C57BL/6J mice, suggesting that HDL in the susceptible strain has a lower cholesterol-carrying capacity. This conclusion is consistent with the observation that the HDL particle size is smaller for C57BL/6J mice than for C3H/HeJ. Both strains increased their apoE levels when fed the synthetic high fat diet, but C3H/HeJ mice had higher levels of apoE on both diets. The major response to consumption of the high fat diet for both strains was an increase in apoB-48 from 5 micrograms/ml on a low fat diet to 54 and 109 micrograms/ml for C57BL/6J and C3H/HeJ, respectively. ApoB-100 showed minimal response to the high fat diet. The defined high fat diet can be used to study atherosclerosis in the mouse since it produces aortic lesions but reduces or eliminates other pathological changes such as gallstone formation and liver damage.
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PMID:Synthetic low and high fat diets for the study of atherosclerosis in the mouse. 238 Jun 34

A single 51-member kindred, ascertained on the basis of a normotriglyceridemic proband with depressed high-density lipoprotein cholesterol (HDL-C) and myocardial infarctions at ages 40 and 42, was studied with respect to quantitative variation in HDL-C and apolipoprotein (apo) AI and AII levels. The results of bivariate segregation analysis suggest that the etiology of depressed HDL-C involves one or possibly two major loci: one has a pleiotropic effect on apo AI and apo AII levels and, possibly another one that affects apo AI levels. Both the major loci were characterized as having a dominant allele leading to depression of the respective trait(s). In addition, analysis of the cosegregation of HDL-C and apo AI levels gave evidence of residual nonfamilial factors common to both traits, leading to a positive covariance between them. This could reflect the role of apo AI in the transformation of nascent HDL-C particles into mature ones via its cofactor activity to lecithin cholesterol acyltransferase. The proposed two-locus model represents one possible etiology for the heterogeneous disorder of hypoalphalipoproteinemia. This analysis of a single pedigree does not completely define the genetic mechanism, but it does illustrate a useful new analytic approach.
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PMID:Genetic factors influencing apolipoprotein AI and AII levels in a kindred with premature coronary heart disease. 314 39

Platelet aggregation, [14C]serotonin release and platelet malondialdehyde production were determined in a patient with abetalipoproteinemia (ABL) and found to be normal. The patient demonstrated complete absence of apolipoprotein (apo) B and decreased apo A-I concentration in plasma. The high density lipoprotein (HDL) composition of plasma was abnormal, with an increased cholesterol/protein ratio, increased apo E levels and reduced apo C concentration. The patient's platelets, like platelets derived from a normolipidemic control, possessed receptors capable of binding lipoproteins. On incubating washed platelets derived from a control subject with HDL obtained from the ABL patient, an enhancement in platelet function was observed. A similar concentration of HDL derived from the control had the opposite effect, a depression of platelet function. Lipoprotein-deficient plasma (LPDP) derived from the patient, on the other hand, decreased platelet aggregation and [14C]serotonin release in comparison to the LPDP obtained from the control. The normal platelet function observed in the patient appears to be the result of the platelet-enhancing effect of an abnormal HDL, thus compensating for the absence of low and very low density lipoproteins from the patient's plasma which, when present, stimulate platelet function.
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PMID:Platelet function in a case with abetalipoproteinemia. 408 61

The apolipoprotein epsilon4 allele and homozygous deletion allele (DD) of the angiotensin-converting enzyme gene are reported to be associated with an increase in the incidence of ischemic heart disease. In this study, we examined whether the apolipoprotein epsilon4 genotype and angiotensin-converting enzyme/DD allele are associated with silent myocardial ischemia. We screened 3920 subjects undergoing general checkups who no symptoms of ischemic heart disease. Seventy subjects (2 percent) showed ischemic ST-segment depression during the double two-step exercise test. One hundred and twenty control subjects without ischemic ST-segment depression were recruited from the same population and matched for sex, age, and blood pressure. We performed genotyping of the apolipoprotein E gene (epsilon2, epsilon3, and epsilon4) and angiotensin-converting enzyme gene (I and D) using polymerase chain reaction-restriction fragment length polymorphism and polymerase chain reaction, respectively. Allele frequently of epsilon4 of the apolipoprotein E gene was higher in the ischemic group (11 percent) than the nonischemic group (5 percent) (chi2 = 5.35, P < .05), but there was no significant association between the allele or the genotype frequency of the angiotensin-converting enzyme gene and the incidence of ischemic ST-segment depression. Furthermore, stepwise multiple regression analysis also revealed that total cholesterol level and epsilon4 genotype were predictors of ischemic change in the exercise tolerance test (chi2 = 12.8, P < .005, R(2) = .051). These results suggest that the apolipoprotein epsilon4 allele is an independent genetic risk factor for silent myocardial ischemia in Japanese subjects.
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PMID:Polymorphism of the apolipoprotein E and angiotensin-converting enzyme genes in Japanese subjects with silent myocardial ischemia. 864 25

We followed weekly the evolution of serum lipid concentrations in two bodybuilders undergoing a cycle of treatment with anabolic steroids. These drugs caused maximum depression of high-density lipoprotein cholesterol concentrations by 69.1% in the fifth week after the beginning of the cycle for subject 1, and by 72.4% in the fourth week for subject 2. Maximum increases in low-density lipoprotein cholesterol concentrations were 144% and 156%, respectively. Total cholesterol and apolipoprotein (apo) B were highly increased with anabolic steroid use. We also saw depression of apo A-I by 84% and 91%, and lipoprotein(a) decreased to undetectable amounts in both cases. These effects were reversed 10 weeks after the end of the steroid cycle in subject 1, but subject 2 still presented abnormal concentrations of serum lipids 13 weeks after drug cessation. The periods until reversibility of anabolic steroid effects on lipids were longer than those reported in previous studies.
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PMID:Evolution of serum lipids in two male bodybuilders using anabolic steroids. 866 91

We evaluated the frequency of depression and psychosis in 46 patients with AD and 135 control subjects with the apolipoprotein (APO) E3/3 or E3/4 genotype. Patients with AD and the APOE3/4 genotype had a more than threefold increase in the signs of depression and psychosis when compared with either patients with the APOE3/3 genotype or to control subjects. Our preliminary study suggests that the phenotype of AD associated with the epsilon 4 allele is more likely to include psychiatric manifestations.
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PMID:A preliminary study of apolipoprotein E genotype and psychiatric manifestations of Alzheimer's disease. 871 89

This study compared the serum lipid concentrations in 100 patients with major depressive disorder (MDD) with those from 100 matched healthy controls. It was found that the serum total cholesterol concentration in patients with MDD (5.27 +/- 1.18 mmol/L) was significantly lower than the value (6.63 +/- 1.32 mmol/L) in sex-, age-, and weight-matched healthy controls. This significant decrease in serum cholesterol in patients with MDD was noted in both sexes and in all age groups. Patients with MDD, however, had significantly higher HDL cholesterol than matched controls. There were no statistically significant differences in serum concentrations of triglycerides, apolipoprotein (Apo) A1, Apo B, transferrin, and albumin between patients and controls. Clinical recovery of patients with MDD was accompanied by a significant increase in serum total cholesterol from 5.27 +/- 1.18 mmol/L to 6.12 +/- 1.2 mmol/L. These results suggest an association between low serum total cholesterol and depression in both sexes and at all age groups.
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PMID:Serum lipid concentrations in patients with major depressive disorder. 893 15

High-physical activity levels are associated with reduced risk of symptomatic coronary artery disease (CAD). However, there are a number of reports of exercise-related sudden death and myocardial infarction in aerobically trained athletes. This study compared the prevalence of exercise-induced silent myocardial ischemia on maximum graded exercise tests with tomographic thallium scintigraphy in 70 master male athletes (63 +/- 6 years, mean +/- SD) (maximum aerobic capacity, VO2max >40 ml/kg/min) and in 85 healthy untrained men (61 +/- 7 years) with no history of CAD. The prevalence of silent ischemia (exercise-induced ST-segment depression on electrocardiogram and perfusion abnormalities on thallium scintigraphy) was similar in athletes and untrained men; 16% of the athletes (11 of 70) had silent ischemia compared with 21% of the untrained men (chi-square = 0.81, p = 0.36). No athletes had hyperlipidemia, systemic hypertension, or diabetes mellitus. However, the apolipoprotein E4 allele was present in 9 of the 11 athletes with silent ischemia compared with 2 of 32 athletes with normal exercise tests (chi-square = 24, p = 0.0001). These results suggest that older male athletes with the apolipoprotein E4 allele are at increased risk for the development of exercise-induced silent ischemia.
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PMID:Exercise-induced silent myocardial ischemia in master athletes. 946 64


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