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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The state of carbohydrate metabolism was studied under conditions of endogenous hyperlipemia induced by triton WR-1339. The data obtained testify to the fact that administration of triton WR-1339 to experimental animals intensifies lipogenesis from carbohydrates, that is confirmed by a decrease in the glycogen amount in the liver and by an activation of the pentose-phosphate pathway of carbohydrate oxidation which is important for cells intensely synthetizing fatty acids. Thus, there is a relation between disturbances in carbohydrate metabolism and development of hyperlipemia induced by the triton.
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PMID:[Carbohydrate metabolism and endogenous hyperlipemia]. 72 96

Methodologies for T and B lymphocyte quantitation, lymphocyte blast transformation (LBT) and carbohydrate (CHO) metabolism are important for assessing host lymphocyte response in the clinical laboratory. Modifications of methods for each of these techniques are presented. Results from studies of normal ambulatory adults, patients with diabetes mellitus, sickle cell disease and hyperlipidemia are reported. LBT of normal lymphocytes before and after ethanol exposure are examined. LBT during pregnancy is evaluated. T cell populations are abnormally high in black diabetics and decreased in patients with sickle cell anemia. B cell subpopulations are increased in patients with sickle cell anemia. LBT responses are decreased in maturity onset diabetes, during pregnancy and in patients with sickle cell disease. Ethanol in amounts attainable during human consumption results in significantly decreased LBT response. CHO metabolism (especially hexose monophosphate shunt [HMPS] and HMPS by pentose sugar recycling) is abnormal in diabetic lymphocytes. The low HMPS activity is partially reversible by treatment with prostaglandin synthetase inhibitors. Information related to lymphocytes in normal states remains to be collected by further clinical application of these techniques of quantitation and in vitro function.
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PMID:B and T lymphocytes: quantitation, function, and clinical applicability. 696 70

The glycogen storage disorders (GSD)-I, -III, -VI and -VIII are associated with hypertriglyceridaemia or mixed hyperlipidaemia which poses the question whether these patients have an increased risk for atherosclerosis. The atherogenicity of triglycerides has remained controversial, while increased plasma cholesterol levels are generally accepted as a significant risk factor for coronary heart disease. However, clinical data show that one has to differentiate between metabolic conditions where triglycerides are atherogenic and those which are not significantly related to early onset of atherosclerosis but may cause other disorders such as pancreatitis. Among the disorders of carbohydrate metabolism patients with diabetes mellitus frequently have enhanced plasma triglycerides associated with a higher risk for coronary heart disease, while patients with certain types of glycogen storage disease have high triglyceride levels but do not seem to have an enhanced risk for atherosclerosis. Here we have compared the biochemical abnormalities and the atherogenic risk of three different disorders of glucose metabolism including GSD-I (glucose-6-phosphatase deficiency), favism (glucose-6-phosphate dehydrogenase deficiency), and diabetes mellitus which are related to either hyper- or hypolipidaemia. The available data indicate that glucose-6-phosphate (Glc-6-P) is a central molecule in cellular glucose metabolism which critically influences pentose phosphate cycle activity and, via NADPH2-generation, regulates glutathione peroxidase activity for radical detoxification and also cholesterol and triglyceride synthesis. Radical detoxification is a major protective factor for cell membrane integrity and together with an appropriate renewal of membrane lipids may protect against the development of atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose-6-phosphate: a key compound in glycogenosis I and favism leading to hyper- or hypolipidaemia. 831 30

The metabolic changes that accompany changes in Cardiopulmonary testing (CPET) and heart failure biomarkers (HFbio) are not well known. We undertook metabolomic and lipidomic phenotyping of a cohort of heart failure (HF) patients and utilized Multiple Regression Analysis (MRA) to identify associations to CPET and HFBio test performance (peak oxygen consumption (Peak VO2), oxygen uptake efficiency slope (OUES), exercise duration, and minute ventilation-carbon dioxide production slope (VE/VCO2 slope), as well as the established HF biomarkers of inflammation C-reactive protein (CRP), beta-galactoside-binding protein (galectin-3), and N-terminal prohormone of brain natriuretic peptide (NT-proBNP)). A cohort of 49 patients with a left ventricular ejection fraction < 50%, predominantly males African American, presenting a high frequency of diabetes, hyperlipidemia, and hypertension were used in the study. MRA revealed that metabolic models for VE/VCO2 and Peak VO2 were the most fitted models, and the highest predictors' coefficients were from Acylcarnitine C18:2, palmitic acid, citric acid, asparagine, and 3-hydroxybutiric acid. Metabolic Pathway Analysis (MetPA) used predictors to identify the most relevant metabolic pathways associated to the study, aminoacyl-tRNA and amino acid biosynthesis, amino acid metabolism, nitrogen metabolism, pantothenate and CoA biosynthesis, sphingolipid and glycerolipid metabolism, fatty acid biosynthesis, glutathione metabolism, and pentose phosphate pathway (PPP). Metabolite Set Enrichment Analysis (MSEA) found associations of our findings with pre-existing biological knowledge from studies of human plasma metabolism as brain dysfunction and enzyme deficiencies associated with lactic acidosis. Our results indicate a profile of oxidative stress, lactic acidosis, and metabolic syndrome coupled with mitochondria dysfunction in patients with HF tests poor performance. The insights resulting from this study coincides with what has previously been discussed in existing literature thereby supporting the validity of our findings while at the same time characterizing the metabolic underpinning of CPET and HFBio.
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PMID:Metabolic modulation predicts heart failure tests performance. 3122 Jan 3

This study aimed to investigate the protective mechanism of common buckwheat (Fagopyrum esculentum Moench.) against nonalcoholic fatty liver disease (NAFLD) associated with dyslipidemia in mice that were fed a high-fat and high-cholesterol diet (HFD). Results showed that oral supplementation of common buckwheat significantly improved physiological indexes and biochemical parameters related to dyslipidemia and NAFLD in mice fed with HFD. Furthermore, the HFD-induced reductions in fecal short-chain fatty acids were reversed by common buckwheat intervention, which also increased the fecal bile acid (BA) abundance compared with HFD-induced hyperlipidemic mice. Liver metabolomics based on ultraperformance liquid chromatography-quadrupole time-of-flight mass spectrometry demonstrated that common buckwheat supplementation made significant regulatory effects on the pentose phosphate pathway, starch and sucrose metabolism, primary BA biosynthesis, and so forth. The results of high-throughput sequencing revealed that common buckwheat supplementation significantly altered the structure of the intestinal microbiota in mice fed with HFD. The correlations between lipid metabolic parameters and intestinal microbial phylotypes were also revealed by the heatmap and network. Additionally, common buckwheat intervention regulated the mRNA expressions of genes responsible for liver lipid metabolism and BA homeostasis, thus promoting BA synthesis and excretion. These findings confirmed that common buckwheat has the outstanding ability of improving lipid metabolism and could be used as a potential functional food for the prevention of NAFLD and hyperlipidemia.
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PMID:Protective Mechanism of Common Buckwheat (Fagopyrum esculentum Moench.) against Nonalcoholic Fatty Liver Disease Associated with Dyslipidemia in Mice Fed a High-Fat and High-Cholesterol Diet. 3238 65