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

Twenty-two patients suffering from hyperlipidemia and receiving therapy consisting of a lipid-lowering diet and clofibrate (1 g X 2) were in addition given colestipol hydrochloride (5 g X 3) (Colestid, Upjohn) in a randomized, cross-over study for 2 periods of 6 weeks. Both the cholesterol and the triglyceride concentrations in very low density lipoproteins remained unchanged during the colestipol treatment. The cholesterol concentration in low density lipoproteins decreased by 23% (P < 0.001) and increased in high density lipoproteins by 4% (P < 0.01). In a second part of the project, the effects on the lipoprotein lipids of 15 g of colestipol divided into 1, 2 or 3 daily doses were studied when added to ongoing therapy with clofibrate (1 g X 2) and lipid-lowering diet. When the colespitol was divided into 2 or 3 daily doses, the effects were manifested equally but were less pronounced when 1 dose per day was given. In a third study, 14 patients who were treated with a combination of lipid-lowering diet, clofibrate (1 g X 2) and colestipol hydrochloride (15 g daily) were followed over a 2-year period, during which time the serum cholesterol and triglyceride concentrations were maintained at a reduced level. The fasting blood glucose and serum insulin concentrations were increased during colestipol treatment. Such treatment should therefore not be given to patients with impaired glucose tolerance.
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PMID:The effects of colestipol when combined with clofibrate in the treatment of severe hyperlipidemia. Short-term and long-term studies. 700 89

In psoriatic patients with hyperlipidemia we studied the hepatic lipid synthesis from (1-(14)C)-acetate in human liver biopsy specimens in vitro by a thin-layer radio-chromatography. In psoriatics type IV (according to Fredrickson) a significant increase in (1-(14)C)-acetate hepatic incorporation especially into phospholipids (25%) and triglycerides (52%) was observed; in type IIb increased lipogenesis was phospholipids (24.5%), free cholesterol (44.4%) and triglycerides (29%). Abnormal lipid metabolism often coexists with glucose intolerance in psoriasis; no correlation between hyperinsulinemia and augmented (1-(14)C)-acetate incorporation into hepatic triglycerides was found.
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PMID:Lipid synthesis from the liver in patients with psoriasis. 701 Dec 16

The clinical and epidemiological literature is reviewed as to metabolic effects of oral contraceptives (OCs). Both the estrogens and the progestins in OCs cause biochemical alterations which have metabolic consequences. Changes in glucose, lipid, and protein metabolism suggest that the dosage of both estrogens and progestins should be minimized as much as possible. All studies with OCs show no changes in glucose tolerance, but all do consistently show elevated plasma insulin levels as a result of OC usage. This occurs because the pill causes a decrease in insulin sensitivity in healthy women. Increases in age and weight, regardless of OC usage, will also cause an increase in glucose tolerance. Oral glucose tolerance deteriorates in all OC user groups, the greatest deterioration being in the high-dose estrogen users. Women with a history of gestational diabetes or impaired glucose tolerance should be considered high-risk pill users. Lipid abnormalities as a result of pill usage are primarily due to estrogen content. Fasting triglyceride levels are increased in all estrogen users. High-risk factors to be considered in OC prescription are: moderate obesity; diabetes; history of gestational diabetes; hypertension; history of pancreatitis, gallbladder or liver disease; physical evidence of xanthomatosis; age over 30 and smoker; age over 35; family history of hyperlipidemia; and family history of early atherosclerotic vascular disease. Many of the pill-induced protein synthesis changes are similar to those which occur during pregnancy. These, too, are due to estrogen content.
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PMID:Metabolic effects of the birth control pill. 702 12

Chromium deficiency may cause insulin resistance, hyperinsulinemia, impaired glucose tolerance, and hyperlipidemia, recovered by chromium supplementation. The effect of chromium supplementation on serum lipids and glucose tolerance was tested in a double-blind 12-wk study of 23 healthy adult men aged 31 to 60 yr. Either 200 micrograms trivalent chromium in 5 ml water (Cr) or 5 ml plain water (W) was ingested daily 5 days each week. Half the subjects volunteered for glucose tolerance tests with insulin levels. At 12 wk high-density lipoprotein cholesterol increased in the Cr group from 35 to 39 mg/dl (p less than 0.05) but did not change in the water group (34 mg/dl). The largest increase in high-density lipoprotein cholesterol and decreases in insulin and glucose were found in those subjects having normal glucose levels together with elevated insulin levels at base-line. The data are thus consistent with the hypothesis that Cr supplementation raises high-density lipoprotein cholesterol and improves insulin sensitivity in those with evidence of insulin resistance but normal glucose tolerance.
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PMID:Effect of chromium chloride supplementation on glucose tolerance and serum lipids including high-density lipoprotein of adult men. 703 73

Diuretics have been used to treat hypertension since 1958. The doses used were relatively high. Dose-dependent side effects and the increasing availability of other drugs such as beta- and alpha-blockers, calcium-entry blockers, and angiotensin-converting enzyme (ACE) inhibitors, with equal antihypertensive efficacy but additional effects in cardiovascular diseases, led to a decrease in diuretic use. In controlled trials, little or no protection against coronary artery disease (CAD) was discussed as being due to the diuretics' side effects. The main side effects are hypokalemia, hyperglycemia, and hyperlipidemia. Hypokalemia occurs most often (up to 30%) in thiazide-treated hypertensive patients, and may cause arrhythmias in patients with CAD. This side effect is clearly dose-dependent and may be avoided by comedication with antikaliuretics. Glucose intolerance may develop in about 3% of diuretic-treated men and is reversible after discontinuation of the diuretic. This side effect is functionally correlated with hypokalemia and therefore is not seen when patients are given a comedication (for example, spironolactone prevents hypokalemia). Hypercholesterolemia was first reported in 1964 during long-term diuretic treatment. During the first 12 weeks of treatment, low-density lipoprotein (LDL) cholesterol increased 5-15% in men and postmenopausal women. After 1 year of therapy, the levels decreased to pretreatment values. However, in placebo-controlled trials, the placebo groups exhibited cholesterol levels falling below the diuretic group. Although the mechanisms and the clinical implications of these side effects are not completely understood, the perception grew that diuretics per se may have been at least partially responsible for the lack of protection against CAD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of low-dose diuretics in essential hypertension. 750 54

Hypertension is a major contributor to cardiovascular disease, which imparts a threefold increased risk over that of normotensive persons the same age. It accelerates atherogenesis-promoting premature coronary disease, now its most common sequela. The effect of elevated blood pressure on cardiovascular disease morbidity and mortality in general and on coronary disease incidence in particular is independent of the influence of other predisposing atherogenic cofactors but is greatly affected by them. Elevated blood pressure is more often than usual associated with hyperlipidemia, hyperglycemia, hyperuricemia, excessive weight, elevated fibrinogen, and electrocardiogram (ECG) abnormalities, which enhance its impact. Hypertensive coronary candidates usually have an increased low-density lipoprotein/high-density lipoprotein (LDL/HDL) cholesterol ratio, impaired glucose tolerance. ECG abnormalities, or a cigarette smoking habit. These coexisting risk factors exert a greater influence than the character of the blood pressure elevation. Those at risk for hypertensive stroke have left ventricular hypertrophy (LVH), atrial fibrillation, cardiac failure, coronary disease, diabetes, or a cigarette habit. Cardiovascular risk ratios for hypertension diminish with advancing age, but this is offset by a higher absolute risk, making hypertension an important precursor of cardiovascular disease in the elderly.
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PMID:Hypertension as a risk factor for cardiac events--epidemiologic results of long-term studies. 769 48

Based on the analysis of fat distribution by CT scanning, we have proposed a classification of obesity--visceral fat obesity--in which fat accumulation is predominant in the intraabdominal cavity. This type of obesity is more frequently accompanied by disorders of glucose and lipid metabolism and also with hypertension than subcutaneous fat obesity. We also showed that visceral fat obesity was present in almost 90% of obese patients with ischemic heart disease. From clinical and basic experiments, aging imbalance of sex hormone, overintake of sucrose, and lack of physical exercise have been suggested to be major factors for visceral fat accumulation. Since intraabdominal fat (mesenteric and omentum fat) have been shown to have high activities of both lipogenesis and lipolysis, its accumulation induces high contents of free fatty acids, a product of lipolysis, in portal circulation which goes into the liver directly. Excess free fatty acid may cause the enhancement of lipid synthesis and gluconeogenesis as well as insulin resistance, resulting in hyperlipidemia, glucose intolerance, and hypertension and finally atherosclerosis.
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PMID:Pathophysiology and pathogenesis of visceral fat obesity. 769 82

The effects of fructose loading on the integrated cardiovascular function in vivo, glycemic control, glucose tolerance, and plasma lipid levels in nondiabetic and streptozotocin (STZ) diabetic rats were investigated. Endothelial morphology of the thoracic aorta was also assessed with scanning electron microscopy. Fructose-loaded nondiabetic rats exhibited elevated blood pressure and pulse rate, and signs of arterial atherogenesis, such as focal adherence of leukocytes and fibrin to the endothelium. Intraperitoneal glucose tolerance tests revealed a greater increase in plasma insulin in response to glucose challenge in these animals than in the control. Compared with the untreated STZ-diabetic animals, fructose-loaded diabetic rats had significantly greater hyperglycemia, glucose intolerance, and hyperlipidemia and higher blood pressure, but had a similar degree of hypoinsulinemia, cardiac dysfunction, and cardiac enlargement. They also showed signs of early atherogenesis. The central venous pressure and the susceptibilities of the rats to the induction of ventricular arrhythmias by intravenous infusion of aconitine were not significantly affected by either STZ injection or fructose loading. It is concluded that prolonged intake of an excessive amount of fructose has detrimental effects on the cardiovascular system, glucose metabolism, and plasma lipid levels in both nondiabetic and STZ-diabetic rats.
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PMID:Fructose loading induces cardiovascular and metabolic changes in nondiabetic and diabetic rats. 782 85

Glucose intolerance or diabetes mellitus, hyperlipidemia, obesity and hypertension may have a close interrelation based on insulin resistance. We selected 28 impaired glucose tolerance (IGT) patients with hyperlipidemia. The IGT patients demonstrated hypertriglyceridemia associated with hyperinsulinemia, a typical manifestation of insulin resistance. Administration of bezafibrate at 400 mg/day for 4 weeks to the IGT patients with hypertriglyceridemia resulted in an improvement of the plasma glucose level and insulin response to 75 g oral glucose loading associated with a concomitant decrease in non-esterified fatty acids. The ratio of the level of serum C-peptide to that of insulin after a 75 g oral glucose tolerance test (OGTT) was augmented after 4 weeks of bezafibrate administration. However, reduction of the cholesterol level with pravastatin did not alter these parameters. These results suggest that treatment to reduce the level of serum triglycerides, but not that of cholesterol, may have a beneficial effect for improving insulin resistance even in the non-obese subjects with IGT and decreasing the risk of coronary heart disease.
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PMID:Improvement of glucose tolerance by bezafibrate in non-obese patients with hyperlipidemia and impaired glucose tolerance. 785 Dec 75

Insulin resistance or hyperinsulinemia should play an important role in the formation of obesity-associated complications such as hypertension, impaired glucose tolerance, hyperlipidemia etc.. Moreover, obesity is a major aggravating factor for the musculoskeletal disorders. Using the ratio of fasting plasma glucose per insulin (IRI) as a parameter of insulin resistance, I have attempted to know how the insulin resistance would be improved concomitant to the weight reduction of obese patients who mainly suffered from musculoskeletal diseases. The results clearly showed the vigorous weight reduction conducted the significant decrease of the insulin resistance as well as normalizations of blood pressures and several biochemical parameters.
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PMID:[Treatment of obesity as an insulin resistance]. 785 33


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