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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve male M. fascicularis monkeys were divided into two groups of 6 animals each. One group (BASAL) was fed a diet containing 24% protein, 38% carbohydrate and 20% fat, while the other group (ATHER) received an identical diet with the addition of 4.08 g/kg diet cholesterol. The animals were studied over a 4-year period. Blood samples were regularly collected, ECGs taken and carotid artery status evaluated by duplex ultrasound scanning. Lipid xanthomas were monitored by visual inspection. The ATHER group experienced a rapid and sustained rise in serum total cholesterol, concomitant with depression of HDL-cholesterol. In general, triglycerides were significantly higher in ATHER animals. Routine clinical analysis revealed lower hematocrit and hemoglobin, and elevated BUN and alkaline phosphatase in the treated group. Lipid xanthomas were detected early in the ATHER animals, progressing until infiltration was evident on the entire body surface. There were no differences in ECGs between the groups. At approximately 17 months posttreatment, stenosis was apparent in the carotid arteries of treated animals, rising to an average of 90% at study termination. These results indicate that diet-induced carotid atherosclerosis can be monitored non-invasively in the primate with minimum risk to the animal.
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PMID:Clinical profile of a 4-year primate atherosclerosis model. 268 88

We have evaluated the effects of dextrofenfluramine treatment on body weight control during a 90 day period, in obese patients on a calorie-restricted diet. The weight loss in dextrofenfluramine-treated patients was significantly higher than in placebo group. The rate of weight loss was linear up to the end of the trial in d-fenfluramine patients. Neural disturbances (vertigo, headache, depression) were the most frequent side effects observed in both the d-fenfluramine and in the placebo-treated groups, without significant differences between the groups. A total number of 23 patients in the dextrofenfluramine group and 20 patients in the placebo group complained side effects. Six patients (five in the d-fenfluramine group and one in the placebo group) discontinued the treatment, due to the side effects. No modifications of the biochemical parameters considered (fasting blood glucose, bilirubin, alkaline phosphatase, creatinine, blood cell counts, asparate-amino transferase (AST), alanine-amino transferase (ALT), total plasma and HDL cholesterol, and triglycerides) were observed at the end of the trial. A significant reduction of total serum cholesterol was observed in both groups at the end of the period of treatment. In conclusion, dextrafenfluramine was proved to be in short term trials an effective and safe tool in overweight control in obese patients.
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PMID:Efficacy and safety of dexfenfluramine in obese patients: a multicenter study. 305 15

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

Atherogenous dislipoproteinemia, involving a decrease in HDL cholesterol and 3-4-fold increase in the atherogeneity index was found to develop in rats after emotional-pain-dependent stress. Lipid peroxidation was activated in liver tissue of the animals, which was expressed as an increase in the MDA content, a decrease in SOD activity and as marked activation of fructose I-phosphate aldolase, an enzyme specific for liver tissue, in blood serum. The impairment of liver tissue caused an inhibition of 7 alpha-cholesterol hydroxylase--key enzyme of cholesterol hydroxylation into bile acids; the phenomenon may be of importance in development of dislipoproteinemias. Preadaptation of the animals to moderate hypoxia as well as administration of an antioxidant ionol prevented the activation of lipid peroxidation in liver tissue, liberation of fructose I-phosphate aldolase into blood, depression of 7 alpha-cholesterol hydroxylase and protected against the stress-dependent atherogenous dislipoproteinemia. Possible chemical and adaptational protection of liver, which is a very stress-sensitive tissue, is discussed.
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PMID:[Prevention of atherogenic dislipoproteinemias and metabolic disorders in the liver in emotional-pain stress]. 323 31

Using data from Lipid Research Clinics study participants at visit 2 (3972 and 2346 adult men and women), we examined the hypothesis that parental mortality from cardiovascular disease (CVD) or cancer before age 60 predicts their adult progeny's lipid and lipoprotein levels. Weighted regression analysis was used to control for the potential effect of progeny's other CVD risk factors (age, systolic blood pressure, Quetelet index, cigarette smoking, and alcohol consumption), and to assess for the effect of progeny's parental cause-specific mortality status on progeny's lipids and lipoproteins. Nearly all of the statistically significant parent-progeny predictions were for sons. Paternal death from CVD before age 60 years was associated with significantly higher plasma total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels in sons and (at marginal significance) in daughters, when compared with those in reference progeny with paternal survival over age 60 or over age 75. Maternal death from CVD before 60 was associated with lower levels of high-density lipoprotein cholesterol (HDL-C) in sons. Paternal and maternal death from cancer before age 60 years were associated with higher triglyceride levels in adult sons than in sons whose parents had lived beyond ages 60 and 75. Paternal all-cause mortality before age 60 was associated with higher cholesterol and triglycerides in sons; maternal all-cause mortality before age 60 was associated with depression of HDL-C in sons. Familial aggregation of lipids and lipoproteins may account, in part, for familial aggregation of CVD. Knowledge of family history facilitates identification of progeny at higher risk for CVD by virtue of elevated cholesterol or LDL-C, or reduced HDL-C.
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PMID:Progeny's lipid and lipoprotein levels by parental mortality. The Lipid Research Clinics Program Prevalence Study. 394 Jun 84

Forty-six elderly patients (mean age 60 years) suffering from diabetes mellitus (DM), or essential or arteriosclerotic hypertension (HT) were divided into 4 groups. Group 1 served as a control, group 2 was administered 1500 mg niceritrol, group 3 was administered 162 mg acetylsalicylic acid (ASA), and group 4 was administered both 1500 mg niceritrol and 162 mg ASA/day for 8 weeks. Niceritrol lowered serum levels of beta-lipoprotein and total cholesterol and increased HDL cholesterol, usually in 8 weeks. ASA did not affect the lipid-lowering effects of niceritrol. Platelet aggregation induced by epinephrine (1 microgram/ml), collagen (1 microgram/ml), and ADP (2 microM) was depressed in groups 2, 3 and 4. Degrees of depression were higher in groups administered ASA (groups 3 and 4) than in the group administered niceritrol alone (group 2). Plasma fibrinogen levels were lowered in groups administered niceritrol (groups 2 and 4) in 8 weeks. Apparent whole blood viscosity measured at shear rates of 37.6/s and 376/s was improved only in group 4 in 8 weeks, while hematocrit did not change during the study. Because flushing, the most frequent side effect of niceritrol, can be easily controlled by a low dose of ASA, and because the combination of the 2 drugs has some beneficial effects on blood rheology, this combination is considered worthwhile for treatment and prevention of atherosclerosis.
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PMID:The effects on lipids, blood viscosity and platelet aggregation of combined use of niceritrol (Perycit) and a low dose of acetylsalicylic acid. 400 83

Lipids and lipoproteins were measured in 139 men and 145 women who were noninsulin-dependent diabetics (NIDDs) aged 45 to 64 years. Of these, 27 men and 16 women had had a previous definite myocardial infarction (MI). The NIDDs with MI (MI+) showed lower values of HDL and HDL2 cholesterol concentrations than NIDDs without previous MI (MI-) or NIDDS without any symptoms or electrocardiographic signs of coronary heart disease (CHD-). The inverse relationship between HDL, HDL2, and CHD was evident in both sexes, but it was particularly strong among male NIDDs. The difference in HDL and HDL2 cholesterol concentrations between the MI+ and MI- groups or between the MI+ and CHD- groups persisted after adjustment by analysis of covariance for the effect of physical activity, alcohol intake, obesity, duration of diabetes, and glycemic control. It is concluded that in a cross-sectional study, even among NIDDs with generally low HDL and HDL2 cholesterol concentrations, the presence of CHD is associated with a further depression of HDL and HDL2 cholesterol levels. Prospective studies are needed, however, to confirm that the association is predictive and not a consequence of CHD.
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PMID:Association of low HDL and HDL2 cholesterol with coronary heart disease in noninsulin-dependent diabetics. 407 98

In order to confirm the principal risk factor of ischemic heart disease (IHD) in diabetes, multivariate analyses were performed. ST depression in electrocardiogram (ST-ECG) and 18 other clinical-laboratory findings (sex, age, duration of diabetes, blood pressure, cholesterol, HDL-cholesterol, triglyceride, etc.) were measured in 70 non-insulin dependent diabetes mellitus patients. ST-ECG findings were divided into five ranges as an index of the severity of IHD, based on the assumption that the degree of ST-ECG would provide a reasonable correlation to the grade of IHD. In partial correlation analysis, the degree of ST-ECG was significantly correlated both to the level of triglyceride (r = 0.455, p less than 0.001) and to blood pressure (r = 0.392, p less than 0.01), but not to the other 16 variables. Three selected variables (blood pressure, triglyceride and atherogenic index) were sufficient to provide a satisfactory discrimination between patients with and without IHD. Five selected variables (sex, blood pressure, triglyceride, atherogenic index and weight index) were sufficient for evaluation of regression. These results suggest that the high level of triglyceride and hypertension are essential risk factors of IHD in diabetes. It is noticeable that the high level of triglyceride is one of the independent risk factors of IHD in diabetes; it does not depend on the degree of control of hyperglycemia or on the other variables.
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PMID:Analyses of risk factors of ischemic heart disease in diabetics--multivariate analyses. 668 May 27

The dietary effect of omega-3 type highly polyunsaturated fatty acid concentrate (PUFA mix) was investigated on cholesterol and triglyceride levels in the serum and liver, and high density lipoprotein cholesterol (HDL-cholesterol) levels in the serum. The PUFA mix prepared from squid liver oil contained about 75% of total omega-3 type fatty acids. In rats fed the normal diet to which 3% PUFA mix was added, the levels of triglyceride, total cholesterol and phospholipid in the serum markedly decreased as compared to rats fed a 3% methyl-oleate diet. However, lipid peroxide values in the liver and serum increased in rats fed PUFA mix-diets. In the hypercholesterolemic rats, a 5% PUFA mix-diet caused growth retardation and a corresponding reduction in food intake. Lipid peroxide in the liver and serum were more elevated in rats fed diets containing 1, 3 and 5% PUFA mix than in rats fed diets containing 5% oleate or 5% linoleate. In all the rats on PUFA mix-diets, there were depression of serum total cholesterol and elevation of serum HDL-cholesterol. The ratio of HDL-cholesterol to total cholesterol increased in proportion to the amounts of dietary PUFA mix. Total cholesterol level in the liver was depressed after PUFA mix feeding.
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PMID:Dietary effect of omega-3 type polyunsaturated fatty acids on serum and liver lipid levels in rats. 686 45

Haemorrhagic anaemia, exposure to altitude and depression of cell respiration are known to increase plasma triglyceride and cholesterol levels. The common triggering mechanism in all 3 instances is oxygen deficiency but mode of action is not known. The present study was intended to investigate whether lipid lowering drugs clofibrate or gemfibrozil could counteract such hypoxic dyslipidaemia in rats induced by altitude exposure. It was unexpectedly found that in normal rats gemfibrozil elevated plasma total cholesterol with an increase in the HDL-cholesterol component whereas clofibrate caused a rise in LDL-cholesterol. Nicotinic acid had no consistent effect. In hypoxia control rats showed an increase in cholesterol and triglyceride level. Both gemfibrozil and clofibrate prevented the rise of triglycerides. Total cholesterol fell in rats treated either with gemfibrozil or clofibrate during altitude exposure, indicating that neither natural nor gemfibrozil-augmented hyper-HDL-aemia could be maintained during oxygen deficiency.
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PMID:Studies on hypoxic dyslipidaemia. Effect of lipid modulating drugs. 696 88


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