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

Elevated blood pressure is a major contributor to cardiovascular disease in general and to coronary heart disease in particular, now its most common sequela. The risk is proportional to the degree of blood pressure elevation, at all ages and in either sex, whether the increased pressure is labile or fixed, diastolic or systolic in character. The effect of blood pressure on cardiovascular disease incidence is independent of the influence of other predisposing co-factors, but the hazard is greatly influenced by them. Elevated pressures are often accompanied by hyperlipidaemia, hyperuricaemia, overweight, hyperglycaemia, elevated fibrinogen values and ECG abnormalities. The risk associated with any degree of elevation of pressure varies greatly, depending on the number and level of these often associated risk factors, and on whether or not there is the indication of target organ involvement. The excess cardiovascular risk in hypertensive persons tends to be concentrated in those with an increased LDL/HDL cholesterol ratio, impaired glucose tolerance, cigarette smokers and those with accompanying ECG abnormalities. Hypertension is best conceptualised as a component of a multivariate cardiovascular risk profile which provides a sound basis for determining urgency for drug treatment. Optimal preventive management of hypertension requires multifactorial correction of all disordered components of the cardiovascular risk profile before occurrence of target organ involvement.
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PMID:Hypertension. Relationship with other risk factors. 372 May 67

Effects of fructose feeding in moderate amounts on lipid metabolism of obese versus lean, and diabetic versus nondiabetic Zucker rats, were studied. Forty pairs of male lean and obese animals were assigned to two dietary groups, fructose and glucose. For each diet, one-half of lean and obese animals were injected with streptozotocin intraperitoneally (i.p.) to induce diabetes, and the other half were injected with buffer i.p. as a nondiabetic control group. After 9 wk of feeding, animals were fasted overnight, decapitated and exsanguinated. Organs were removed and weighed. Blood glucose, insulin, lactic acid, triglycerides, cholesterol, total liver lipids and urinary glucose were determined. Hyperphagia was observed in obese, non-diabetic and lean-diabetic animals. Streptozotocin injection drastically reduced insulin levels, and produced an impairment of growth, hyperglycemia, glucosuria, polydipsia and polyuria. Fructose feeding increased organ weights in kidney, liver and retroperitoneal adipose tissue, regardless of diabetic state. However, lactic acid levels were lower in fructose-fed groups than glucose-fed groups. In obese rats serum triglyceride levels were also lower in fructose-fed groups than in glucose-fed groups. Serum cholesterol was not affected by fructose feeding. The results indicated that fructose feeding did not produce hyperlipemia and lactic acidosis in the blood circulation in Zucker rats. However, fructose feeding did not improve glucose intolerance in diabetic animals, rather fructose feeding produced hyperinsulinemia in nondiabetic, obese animals.
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PMID:Effects of fructose feeding on lipid parameters in obese and lean, diabetic and nondiabetic Zucker rats. 390 Mar 13

A new, spontaneously occurring diabetic syndrome has been observed in the aged males of an inbred strain of Wistar rats, WBN/Kob. The main clinical sign, glycosuria, was first detected at about 60 weeks of age, and thereafter some animals developed hyperlipidaemia and gradual emaciation. Prior to the onset of glucosuria, male rats showed impaired glucose tolerance after a glucose load at 21 weeks of age. The histopathologic lesions of the pancreas in the diabetic males consisted of multifocal fibrosis, decreased in number and size of islets and atrophy of exocrine tissue. Multifocal inflammatory foci of varying stages were the main pancreatic lesion in prediabetic male rats. This inflammatory change was detected even in 12-week-old rats and tended to occur around the islets. Therefore focal fibrosis and the decrease in the number and size of islets were considered to result from post-inflammatory scarring. The maturity-onset of this syndrome and the impaired glucose tolerance in younger animals suggested that diabetes mellitus of this rat strain is insulin-independent type II. However, the histological lesions of the pancreas were somewhat different from previous reports of both type I and II diabetes mellitus in man and animals.
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PMID:A new diabetic strain of rat (WBN/Kob). 403 61

The major premise by which weight reduction is used as a medical therapy is the fact that obesity is a primary risk factor in the onset and severity of many medical diseases. Hypertension, coronary artery disease, adult onset diabetes mellitus, complications of major abdominal and thoracic surgery, cancer of the breast and colon, and degenerative joint disease are prevalent diagnoses. The data to support weight reduction use as a medical therapy derive primarily from studies of cardiovascular disease. These studies show lowering of blood pressure and reduction of risk factors for glucose intolerance, angina, and hyperlipidaemia. The magnitude of weight loss (percent reduction in excess body weight) is important; 10 per cent reduction is a firm threshold in obese patients (greater than 130%- less than 200% ideal body weight). Success at achieving this medical therapy is most frequent using very low calorie diets which average 30-40% reduction of excess body weight. Mild and moderate hypertension will respond in 90% of patients. Type II diabetes mellitus patients can become free of exogenous insulin requirement. Response to general anaesthesia and control of respiratory distress syndrome will improve if preoperative weight loss is achieved. Improved cardiovascular fitness and relief of exertional dyspnoea are other clinically important outcomes of very low calorie diet therapy. A high priority exists to investigate the use of comprehensive professional weight control therapy as medical treatment.
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PMID:Benefits of reducing--revisited. 624 29

We have previously reported that normal Wistar rats fed an isocaloric, sucrose-rich (63%) diet (SRD) developed glucose intolerance and elevated triglyceride levels in plasma as well as in heart and liver tissue. This metabolic state was accompanied by hyperinsulinism both in vivo and in vitro, suggesting that a state of insulin resistance has developed. The aim of this study was to gather information on the various plasma post-heparin lipolytic activities in rats fed a SRD. Hepatic triglyceride lipase (H-TGL) was evaluated by both, protamine sulfate inhibition (PSI) of extrahepatic lipoprotein lipase (LPL) and heparin-Sepharose affinity chromatography (H-SAC). Both methods rendered comparable results. Total triglyceride lipase (T-TGL) was measured after Krauss et al. and monoglyceride hydrolase (MGH) after Vogel et al. Our results have shown a significant decline of plasma T-TGL (5.32 +/- 0.34 means +/- SEM vs. 7.48 +/- 0.64 mumol glycerol ml-1 h-1; p less than 0.01), H-TGL (3.71 +/- 0.28 vs. 5.05 +/- 0.69; p less than 0.05), LPL (1.61 +/- 0.26 vs. 2.42 +/- 0.41; p less than 0.05) and MGH (558 +/- 108 mumol glycerol l-1 min-1 vs. 1,165 +/- 45; p less than 0.001) activities. Thus, feeding a sucrose-rich diet induced a state of hyperlipemia and insulin resistance in which not only plasma T-TGL but also H-TGL and MGH activities were significantly decreased. This suggests that the latter two enzymes are also under nutritional and/or hormonal control.
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PMID:Post-heparin plasma hepatic triglyceride lipase and monoglyceride hydrolase activities in hyperlipemia induced by a sucrose rich diet. 661 28

The purpose of this investigation was to evaluate the benefits and the potential risks of a very low calorie protein-diet in obese patients with metabolic abnormalities and at increased cardiovascular risk. To this end, the 420 kcal diet (with 50% of energy as protein) was administered for 10 days to 10 grossly obese subjects with glucose intolerance, hyperlipemia, arterial hypertension, ischemic cardiopathy and thrombotic risk related to high levels of fibrinogen factor VIII and reduced fibrinolytic activity. Weights loss averaged 360 g/day with a mean protein loss of 17 g/day occurring essentially during the very early phase of the diet. There was a rapid normalisation of blood pressure, plasma lipids and glycaemia. With the exception of a slightly negative potassium balance other ion remained in balance. There was no change in electrocardiogram, in parameters of blood coagulation or in hepatic and renal function. There was only a moderate increase in ketonaemia and plasma urate. It appears therefore, that an 8 to 10 day very low calorie protein-diet is well tolerated even in obese patients with increased cardiovascular risk, and that it corrects of several metabolic abnormalities without alteration in cardiac, hepatic or renal function.
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PMID:[Evaluation of tolerance of a modified protein diet in obese subjects]. 665 61

The follow-up (3 to 20 years, mean = 8,9 yrs) of 145 patients with intermittent claudication showed the high incidence of tobacco use (86%) hyperlipidemia (43%) elevated blood pressure (45%) and glucose intolerance (30%), two or more of these factors were present in 66% of cases. A statistically significant higher rate of fairly reduced risk factors was noted in 57 patients improved functionally (based on the maximal walking distance on treadmill and arm/ankle systolic pressure ratio) versus 45 functionally impaired patients, and in 55 patients free of CHD, compared with 54 patients with coronary events (p 0.001). A group of 26 patients with cerebro-vascular insufficiency exhibited a higher incidence of non reduced hypertensive cases.
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PMID:[Long term follow up of patients with intermittent claudication and correlated with the management of risk factors (author's transl)]. 678 60

Previous studies have suggested an association between hyperlipidaemia and retinal venous and arterial occlusion. To investigate this association further, the retinal arterial vasculature was studied by fluorescein angiography in forty hyperlipidaemic subjects, and clinical examination and biochemical investigations, including lipid profile, were performed in 99 patients with retinal vein occlusion and forty patients without retinal vein occlusion as a comparison group. Retinal arterial abnormalities were found on fluorescein angiography in eight patients with combined hypercholesterolaemia and hypertriglyceridaemia (type IV and V hyperlipidaemia). However no abnormalities were found in patients with familial hypercholesterolaemia (type II). Fluorescein angiography was repeated after 6 months hypolipidaemic therapy in four of the patients with retinal arterial abnormalities. Progression of retinal vascular closure was observed in two patients with poor hyperlipidaemic control and improvement in two other patients with good hyperlipidaemic control. There was a significantly higher incidence of hyperlipidaemia (P less than 0.001) and glucose intolerance (P less than 0.05) in the retinal vein occlusion group when compared to the control group, and a higher incidence of hypertension in patients with either central or branch retinal vein occlusion than in the normal population. We conclude that retinal arterial abnormalities occur in type IV and V hyperlipidaemias and that both central and branch retinal vein occlusion are associated with similar risk factors to large vessel disease.
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PMID:Retinal vascular abnormalities in the hyperlipidaemias. 696 27

Hyperlipidemia associated with an isolated deficiency of growth hormone was investigated in 10 subjects with hypercholesterolemia consistently present over a 10-yr period. 8 of these 10 had serum triglyceride concentrations greater than 185 mg/dl. 13 growth hormone-deficient patients with normal serum lipids, 28 age-matched controls, and 6 families possessing both growth hormone-deficient and hormonally normal members were also studied. Hyperlipidemia occurred with growth hormone deficiency only in families in which hormonally normal subjects likewise exhibited hyperlipidemia. However the elevation of serum lipids, particularly cholesterol, was invariably greater in the growth hormone-deficient members of these families. Studies were most consistent with the classification of this trait as familial combined hyperlipoproteinemia. Basal serum concentrations of insulin, glucose, and free fatty acids were similar in all groups. After oral glucose (1.5 g/kg of body wt) both hyperlipidemic and normolipidemic dwarfs exhibited a similar degree of glucose intolerance associated with insulinopenia. Sensitivity to insulin, assessed after the intravenous injection of insulin (0.05 U/kg of body wt), increased and was virtually identical in the two dwarf groups. Administration of 5 mg of human growth hormone twice a day for 1 wk to five subjects did not alter serum lipid patterns. The data provide no conclusive evidence concerning a direct effect of growth hormone deficiency on hyperlipoproteinemia. We postulate that in some individuals growth hormone deficiency may unmask an underlying defect in lipoprotein metabolism.
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PMID:Familial combined hyperlipoproteinemia. Evidence for a role of growth hormone deficiency in effecting its manifestation. 698 67

In spite of the methodological reserves that the measure of adipocyte volume and the calculation of the number of adipocytes evoke, it appeared interesting to us to study these parameters in a group of 102 obese subjects in reference to some clinical and biological criteria. The following conclusions come out of this study. The greater the obesity, the greater the adipocyte volume. There is a positive correlation between the importance of obesity and cellularity of the adipose tissue. However, this correlation is no longer found for the most obese patients, in whom adipocyte hypertrophy intervenes but no longer the multiplication of the fat cells. The onset of obesity at adolescence pairs with a number of adipocytes higher than in the other chronological forms: obesity appearing at adolescence would be thus more frequently hyperplastic. This characteristic is not discovered in the cases of obesity appearing in infancy. No relation was found between the existence of impaired glucose tolerance and mean adipocyte diameter and/or the number of adipocytes. It has been the same for the cases of hyperlipidemia.
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PMID:[Morphology of adipose tissue. Study in 102 obese subjects in reference to some clinical and biological criteria (author's transl)]. 698 92


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