Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute effects of fatty meals (900 kcal) rich in saturated (cream) or n-3 polyunsaturated (cod liver oil, CLO) fatty acids on human umbilical vein endothelial cells (ECM) and platelet behavior were studied. The ECM were incubated for 24 hours at 37 degrees C with either plasma or chylomicrons (CM) obtained 3 hours after the meals. The ability of the ECM to inhibit platelet aggregation (PIA) and the release of prostaglandin I2 measured as 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured after 24 hours of incubation, after stimulation and after freezing and thawing. Similar studies were done with CM from a patient with type V hyperlipoproteinemia. The release of 6-keto-PGF1 alpha was increased by postprandial plasma and by CM obtained after both meals. Plasma collected after CLO, but not after cream, increased PIA, whereas CM derived from all sources studied stimulated the PIA of ECM. No consistent correlation could be established between the release of 6-keto-PGF1 alpha and PIA. Increased platelet aggregation in platelet-rich plasma was always observed during postprandial hyperlipidemia.
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PMID:Effects of postprandial plasma and chylomicrons on endothelial cells. Differences between dietary cream and cod liver oil. 375 2

There is an abundance of information suggesting that prostaglandins are involved in the development and clinical expression of atherosclerosis. Many studies demonstrate a relationship between prostaglandins and the risk factors for peripheral and coronary artery disease. Thus, part of the mechanism by which hyperlipidemia, diabetes mellitus, smoking, hypertension, sex hormones, age, heredity, emotional stress and diet contribute to the development and progression of atherosclerosis may be through an imbalance between thromboxane A2 and prostaglandin I2. Recent studies show a temporal relationship between acute ischemic events (specifically, unstable angina) and a transcardiac increase in thromboxane B2, while others demonstrate a salutary effect of disaggregatory and vasodilatory prostaglandins in such patients. If prostaglandins and thromboxane prove important in ischemic vascular disease, attention will be directed at the correction of their pathologic imbalance. This may be accomplished by dietary manipulation as well as by the development of prostaglandin receptor antagonists or inhibitors of specific prostaglandin pathways.
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PMID:Prostaglandins and ischemic heart disease. 703 86

Complex traits are often manifested by multiple correlated traits. One example of this is hypertension (HTN), which is measured on a continuous scale by systolic blood pressure (SBP). Predisposition to HTN is predicted by hyperlipidemia, characterized by elevated triglycerides (TG), low-density lipids (LDL), and high-density lipids (HDL). We hypothesized that the multivariate analysis of TG, LDL, and HDL would be more powerful for detecting HTN genes via linkage analysis compared with univariate analysis of SBP. We conducted linkage analysis of four chromosomal regions known to contain genes associated with HTN using SBP as a measure of HTN in univariate Haseman-Elston regression and using the correlated traits TG, LDL, and HDL in multivariate Haseman-Elston regression. All analyses were conducted using the Framingham Heart Study data. We found that multivariate linkage analysis was better able to detect chromosomal regions in which the angiotensinogen, angiotensin receptor, guanine nucleotide-binding protein 3, and prostaglandin I2 synthase genes reside. Univariate linkage analysis only detected the AGT gene. We conclude that multivariate analysis is appropriate for the analysis of multiple correlated phenotypes, and our findings suggest that it may yield new linkage signals undetected by univariate analysis.
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PMID:Comparison of univariate and multivariate linkage analysis of traits related to hypertension. 2001 96