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

Sodium dodecylsulphate precipitates very low density lipoproteins (VLDL and chylomicrons) rich in triglyceride and a narrow correlation (r = 0.9) was found between the turbidimetric index SDS and triglyceridemia. Heparin in calcium medium acts in the same way and precipitates also low density lipoproteins (LDL) rich in cholesterol. A correlation (r = 0.875) was drawn up between the cholesterol LDL and the difference between the turbidimetric indices (heparin Ca -- SDS). In the first case, we were thus measuring by turbidimetry a VLDL + chylomicron index and, in the second case, an LDL index which permits one to obtain simplified typing of the hyperlipoproteinemias. A nomogram linking the two indices of hyperlipoproteinemia type was drawn up experimentally. This orientation analysis may be completed by electrophoresis on polyacrylamide gel used in concentration gradient and pH. In the system proposed, the lipoproteins were previously stained with tetrazolium nitroblue and clearly shown up. The chylomicrons in particular, become separated from the VLDL, the sinking pre-beta-lipoprotein or Lp (a) was identifiable and the type III hyperlipemia was easily diagnosed.
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PMID:[Analysis of lipoproteins using polyacrylamide gel electrophoresis and fractionated precipitation with polyanions and detergents. Use in the classification of hyperlipoproteinemias]. 18 41

Sodium, potassium, and chloride levels are artifactually depressed in hyperlipemic sera. Accurate electrolyte levels are needed for management of patients with hyperlipemia, but present methods for correcting the values (serum water and/or osmolality determinations) either are technically cumbersome or fail to provide accurate data to correct the falsely low levels. Alternatively, to determine true sodium, potassium, and chloride concentrations in hyperlipemic sera, only the required electrolyte values and the triglycerides are measured. The percentage by which the measured electrolyte levels in the hyperlipemic sample must be increased to approximate the true values is given by the following equation: per cent increase = 2.1 X triglycerides (Gm./dl.) - 0.6.
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PMID:A simple and precise method of determining true sodium, potassium, and chloride concentrations in hyperlipemia. 96 12

1. Increased erythrocyte sodium-lithium countertransport activity has been reported to be associated with nephropathy in type 1 diabetes and linked to a family history of essential hypertension. 2. This study aimed to determine the mechanism of increased sodium-lithium countertransport activity. Sodium-lithium countertransport kinetics were measured in uncomplicated and hyperlipidaemic type 1 diabetic patients. 3. In the nine out of 31 uncomplicated type 1 diabetic patients who had high sodium-lithium countertransport activity, the sodium affinity (Km) was normal but the maximum velocity (Vmax) was increased. 4. Hyperlipidaemia, when present in diabetic patients, was associated with increased sodium-lithium countertransport activity, but could not explain the high activity in uncomplicated type 1 diabetic patients in whom plasma lipid concentrations were normal. 5. Sodium-lithium countertransport activity is increased in type 1 diabetes by a mechanism different to that in essential hypertension, where the mechanism is a low Km (increased sodium affinity). Hence familial hypertension cannot explain the raised sodium-lithium countertransport activity in type 1 diabetes.
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PMID:Kinetics of sodium-lithium countertransport activity in patients with uncomplicated type 1 diabetes. 131 14

A survey of dietitians at renal transplant centers in the United States was conducted to identify diet modifications currently used for nondiabetic adults after kidney transplantation. The survey focused on the diet recommended for the first 21 days after successful transplantation. Questionnaires were mailed to 100 centers randomly selected from a comprehensive list obtained through the Organ Transplant Coordinating Office of the Texas Medical Center, Houston. A 66% response rate was obtained. The results of the survey showed that dietitians were most frequently recommending 1.2 to 1.5 gm protein per kg body weight, 40% to 50% of total energy as carbohydrate, a fat intake of less than 30% of total energy, and an energy level consistent with achieving or maintaining desirable body weight. Sodium intake was most commonly restricted to 2 to 4 gm, whereas potassium and phosphorus intakes were individualized according to the patient's serum values. Comments on the returned questionnaires indicated that many institutions were reviewing and updating their transplant diet to include a polyunsaturated fat to saturated fat ratio and restrictions of cholesterol and simple sugars. The findings of the survey indicated that the renal transplant diet should focus on optimal protein and energy intake as well as restriction of simple sugars, total fat, cholesterol, and saturated fat to restore nitrogen balance and minimize clinical symptoms of post-transplant diabetes and hyperlipidemia.
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PMID:Renal transplant diet recommendations: results of a survey of renal dietitians in the United States. 234 58

1. We measured sodium-lithium countertransport, sodium-hydrogen exchange and membrane micro-viscosity in 48 individuals with familial hypercholesterolaemia, 33 subjects with hypertriglyceridaemia and 54 normolipaemic controls. Full lipid profile, blood pressure, body mass index, fasting glucose and insulin levels were also measured. 2. Subjects with hypertriglyceridaemia had higher blood pressure, body mass index, fasting glucose and insulin levels than normal controls. 3. Vmax of the sodium-lithium countertransport was elevated in the hypertriglyceridaemic group compared with controls. Across the whole group log(e) triacylglycerols correlated with Vmax of the sodium-lithium countertransport. There was no difference in sodium-lithium countertransport K(m) between the groups. 4. Sodium-hydrogen maximal proton efflux rate (Vmax) and K(m) were not different between the three groups. There were no correlations between sodium-hydrogen exchange and sodium-lithium countertransport parameters. 5. Microviscosity as measured by diphenylhexatriene was reduced at the core of the membrane in subjects with hypertriglyceridaemia compared with those with familial hypercholesterolaemia or normolipaemic controls, suggesting an alteration in membrane structure. 6. Changes in sodium transport in hyperlipidaemia may be mediated by changes in membrane structure resulting in altered protein conformation or turnover.
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PMID:Sodium-lithium countertransport, sodium-hydrogen exchange and membrane microviscosity in patients with hyperlipidaemia. 909 3

Sodium-lithium countertransport (SLC) in erythrocytes represents one of the transmembrane sodium transport systems. SLC activity is elevated in arterial hypertension, diabetes mellitus type I (IDDM) complicated with nephropathy, hyperlipidemia, hyperuricemia and pregnancy. Increase of SLC is considered as a genetic marker of primary arterial hypertension. In present paper SLC was assessed in 12 patients with IDDM without nephropathy (group I), 12 patients with IDDM complicated with diabetic nephropathy on hemodialytic treatment (group II), 15 patients treated with haemodialysis due to non-diabetic nephropathy (group III) and 12 healthy subjects (group IV). All groups were matched in respect of age. Serum creatinine concentration and inulin clearance were similar in groups I and IV as well as in groups II and III. SLC was assessed according to method described by Canessa and coworkers (1980). SLC activity in group II (0.60 mmol/l litre of erythrocytes/h; 0.43-0.94; 0.28-1.22) (median, 25%-75%, min.-max.) was significantly higher than in other groups-group I (0.30; 0.20-0.38; 0.12-0.57), group III (0.24; 0.16-0.33; 0.11-0.38) and group IV (0.20; 0.15-0.25; 0.12-0.27). In 3 patients of group I the values were higher than in all examined of groups III and IV and approximated to mean values of group II. The results confirm a significant rise of SLC activity in patients with IDDM complicated with end-stage diabetic nephropathy. SLC activity in end-stage renal disease due to non-diabetic nephropathy does not differ from values in healthy subjects. It seems that elevated SLC activity in IDDM might be a genetic marker foretelling development of nephropathy.
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PMID:[Activity of sodium-lithium cotransport in erythrocytes of patients with diabetes mellitus type I (IDDM) complicated by diabetic nephropathy in the renal failure stage]. 944 Dec 88

Sodium-lithium countertransport (SLC) kinetics were measured in 30 patients with type V hyperlipidemia, 30 patients with type IIB hyperlipidemia on similar treatment, and 30 age- and sex-matched healthy controls. Clinical and laboratory data including basic anthropometry and blood pressure were obtained and blood was taken for detailed lipid biochemistry, glucose, insulin, and leptin measurements. Patients with type V hyperlipidemia were normotensive but more obese than controls, had elevated triglycerides, very low-density lipoprotein, glucose, and insulin; and reduced HDL cholesterol compared with type IIb controls. The median SLC activity (0.23 v 0.21 mmol Li+/L RBC/h) and median maximal velocity (0.33 v 0.31 mmol Li+/L RBC/h) were increased, but not significantly, compared to controls. In patients with type V hyperlipidemia SLC maximal velocity correlated with log triglycerides (r2 = 0.853; P < .001) and log very low-density lipoprotein (VLDL) triglycerides (r2 = 0.947; P < .001). Sodium-lithium countertransport maximal velocity correlated weakly with the homeostasis model assessment index of insulin resistance (r2 = 0.224; P = .06). The sodium affinity of the transporter did not differ between the groups and was independent of any of clinical or biochemical parameter studied. We conclude that VLDL triglyceride is strongly correlated with SLC maximal velocity and activity in patients with type V hyperlipidemia.
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PMID:Relation between sodium-lithium countertransport and hypertriglyceridemia in type V hyperlipidemia. 1120 76

A number of epidemiologic and experimental studies have revealed the close relationship between salt intake and blood pressure. The objective of this study was to know the salt intake among 293 not previously treated hypertensive patients and to identify their clinical characteristics that would allow us to define the profile of patients with high sodium intake. Hypertensive patients who first attended a specialized high blood pressure (HBP) clinic not previously treated with drugs, at least for the last month were selected. Sodium 24 h urinary excretion was determined on two occasions, as sodium intake index. Thirteen percent of patients had a salt intake lower than 100 mEq/24 h and 35% of patients higher than 200 mEq/24 h. Sodium intake was higher among men, younger patients, those with a higher Quetelet index, smokers, higher socioeconomic status, and less years with IBP. No differences were observed between salt intake among hypertensive patients with associated diabetes or hyperlipidemia. The Quetelet index, sex, age and smoking were identified as independent variables for salt intake by the multiple linear regression analysis. No correlation was found between salt intake and blood pressure. In conclusion, a high sodium intake was observed in our setting among hypertensive patients who had previously been advised to moderate salt intake. The highest salt intake was observed among men, youths, obese and smokers.
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PMID:[Clinical characteristics of patients with essential hypertension regarding salt intake]. 1178 28

The present work includes a study on the glycosaminoglycanuric condition induced by adriamycin (ADR, a chemotherapeutic agent) and the accompanying secondary hyperlipidemia, wherein the treatment with a low-molecular-weight heparin-derivative (LMWH), certoparin, is evaluated for its protective role (if any) on these parameters. Two groups of male albino rats of the Wistar strain (140+/-10 g) received a single intravenous injection of adriamycin (7.5 mg/kg), and one of these groups was treated with a low-molecular-weight heparin-derivative (Certoparin Sodium, Troparin; 300 microg/day/rat s.c.), commencing on day 8, for a week. Urinary total glycosaminoglycans excretion of the untreated ADR-induced group was found to increase on the 8th and the 15th days of observation, when compared with the controls. The LMWH treatment commencing on day 8 resulted in minimising the glycosaminoglycans (GAGs) excretion by day 15 (p<0.001). Plasma, cardiac, hepatic and renal lipids (cholesterol, triglycerides and phospholipids) showed a sharp increase in the pathologic group, along with a rise in plasma LDL and VLDL cholesterol and drop in HDL cholesterol levels, paralleled by abnormal activities of the enzymes involved in lipid metabolism. LMWH treated group showed a normalised lipid profile and the activities of the lipid-metabolising enzymes was close to that of controls. It is concluded herein that adriamycin administration resulted in severe nephropathy manifested by increased glycosaminoglycanuria and abnormal lipid metabolism, and that LMWH treatment afforded substantial protection by restoring glomerular structure and function, and normalised the plasma and tissue lipid levels, lipoprotein profile and the activities of lipid-metabolising enzymes.
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PMID:Beneficial cardio-renovascular effects of a low-molecular-weight heparin-derivative on adriamycin-induced glycosaminoglycanuria and tissue lipid abnormalities. 1586 50

The worldwide increase in the incidence of metabolic syndrome correlates with marked increase in total fructose intake in the form of high-fructose corn syrup, beverage and table sugar. Increased dietary fructose intake in rodents has been shown to recapitulate many aspects of metabolic syndrome by causing hypertension, insulin resistance and hyperlipidaemia. Recent studies demonstrated that increased dietary fructose intake stimulates salt absorption in the small intestine and kidney tubules, resulting in a state of salt overload and thus causing hypertension. The absorption of salt (sodium and chloride) in the small intestine is predominantly mediated via the chloride/base exchangers DRA (Down Regulated in Adenoma) (SLC26A3) and PAT1 (Putative Anion Transporter 1) (SLC26A6), and the Na(+) /H(+) exchanger NHE3 (Sodium Hydrogen Exchanger3) (SLC9A3). PAT1 and NHE3 also co-localize on the apical membrane of kidney proximal tubule. Luminal fructose stimulated salt absorption in the jejunum and kidney tubules, responses that were significantly diminished in PAT1 null mice. These studies further demonstrated that Glut5 (SLC2A5) is the major fructose-absorbing transporter in the small intestine (and kidney proximal tubule) and plays an essential role in the systemic homeostasis of fructose. Increased dietary fructose intake for several weeks upregulated the expression of NHE3, PAT1 and Glut5 in the intestine and resulted in hypertension in wild-type mice, a response that was almost abolished in PAT1 null mice and abrogated in Glut5 null mice. This article will discuss the interaction of Glut5 with salt-absorbing transporters and review the role of dietary fructose in enhanced salt absorption in intestine and kidney as it relates to the pathogenesis of hypertension in metabolic syndrome.
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PMID:Dietary fructose, salt absorption and hypertension in metabolic syndrome: towards a new paradigm. 2114 27


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